SG F21 Disorders Cardiac Function, Heart Failure, Circulatory Shock

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1 Disorders of Cardiac Function, Heart Failure, Circulatory Shock Study Guide Before you get started … If your memory of normal cardiac A&P is weak, now is the time to review. Understanding normal flow through the heart (and body) will help you understand the clinical manifestations of all of these disorders in this chapter. And understanding is KEY for applying this content to your exam questions. View this video at Khan Academy (14:56, can start at 2:26, stop at 13:43). There’s a lot of stuff in this chapter … let’s get going! Disorders of the Pericardium The pericardium is a double layered serous membrane surrounding the heart; 2 layers – space in between these layers is pericardial sac … contains about 50 ml (about 2 ounces). 1. Compare the pathophysiology and clinical manifestations of acute pericarditis (triad), pericardial effusion (including cardiac tamponade), and constrictive pericarditis (p. 666-668). Acute pericarditis Pericardial effusion + cardiac tamponade Constrictive pericarditis Pathophysiology Inflammation process of the pericardium < 2 week s; most common cause is: Viral infections (e.g., with coxsackieviruses and echoviruses) Associated increased capillary permeability > plasma proteins enter what? leave capillaries and enter the pericardial space Leads to fibrin exudate that heals or leads to what? progresses to scar tissue and forms adhesions between the layers of serous pericardium What is an effusion? accumulation of fluid in the pericardial cavity, usually as a result of an inflammatory or infectious process. It may also develop as the result of neoplasms, cardiac surgery, trauma, cardiac rupture due to MI, and dissecting aortic aneurysm Amount of fluid, how quickly it develops, and elasticity of the pericardium will determine the effects the person will experience. Typically it is 50mL Sudden accumulation of _ 200 _ ml may increase intracardiac pressure that limits venous return to the heart Can lead to Cardiac tamponade – increased intracardiac pressure, Fibrous, scar tissue develops in pericardial sac. Scar tissue contracts and interferes with what? diastolic filling, and CO and cardiac reserve become fixed. Cause: radiation treatments, cardiac surgery, infection

2 Acute pericarditis Pericardial effusion + cardiac tamponade Constrictive pericarditis diastolic filling reduced, cardiac output and stroke volume decreased. Clinical manifestations List the triad. chest pain, pericardial friction rub, and electrocardiographic (ECG) changes (To hear a pericardial friction rub ) What is the pain like? typically worse with deep breathing, coughing , swallowing , and positional changes because of changes in venous return and cardiac filling. Relief when sitting up or leaning forward Manifestations of an effusion: may be asymptomatic unless fluid accumulation is abrupt, then signs of dec. cardiac output. Like: Hypotension, tachycardia, dizziness, fatigue, confusion, weak pulse. Can lead to Cardiac Tamponade VERY SERIOUS: since heart can’t fill or eject properly … Tachy or brady cardia? Increased or decreased cardiac contractility . dizziness, confused, weak pulse, Central venous pressure: Elevated Jugular vein: Distention Systolic BP: Decrease Pulse pressure narrows Heart sounds: muffled Signs of circulatory shock Prominent early finding is what? Ascites + pedal edema, dyspnea on exertion, fatigue Click this link to see Cardiac Tamponade on Grey’s Anatomy (2:53). Will help you remember signs! Cardiac Tamponade is a compression of the heart that is caused by effusion. Results in increase intracardiac pressure, diastolic filling is reduced, cardiac output and stroke volume is decreased. Its very serious because the heart can't eject or fill properly, not getting the supply it needs. We’re moving on to coronary artery disease. This section is full of lots of content. Before we look at disorders, take a look at figure 27-3 on p. 669. The coronary arteries supply oxygenated blood to the myocardium (heart muscle). If they become clogged, there could be serious problems. Coronary Atherosclerosis and the Pathogenesis of Coronary Artery Disease (CAD). What is the most common cause of CAD?

3 2. Describe the pathogenesis of atherosclerosis in terms of stable vs. unstable plaque, and thrombosis with vessel obstruction (p. 671-672). As a reminder from our last chapter, atherosclerosis causes plaque that can obstruct blood flow and can eventually cause a cascade of events that lead to thrombus formation. Stable Plaque: covered by a thick fibrous cap and has a small lipid pool - Stable Angina* Stable (or fixed) plaque: obstructs blood flow, implicated in what? in stable angina and the unstable plaque in UA and MI. Unstable Plaque: has a thin fibrous cap with larger lipid pool - Unstable Angina* & Myocardial Infarction Unstable (or vulnerable) plaque: can rupture and cause what? platelet adhesion and thrombus formation. Plaque disruption can occur spontaneously, but often triggered by hemodynamic factors, such as increased BP, heart rate (HR), cardiac contractility, and coronary blood flow. Why does it often occur during the first hour upon awakening? suggesting that physiologic factors such as surges in coronary artery tone and blood pressure may promote atherosclerotic plaque disruption and platelet deposition Thrombosis and vessel occlusion Plaque disrupts (involves lipid core, smooth muscle cells, macrophages, collagen) > tissue factor released > coagulation pathway initiated > thrombin generated and fibrin deposited Look at figure 27-5 on p. 672. Notice how the lumen changes as the disease worsens? Keep that visual in your mind - it will help this content make sense. Now we’ll dig deeper into acute coronary syndrome and chronic ischemic heart disease as noted in the diagram above, starting with ACS. Acute Coronary Syndrome, includes ● Unstable angina (UA) ● Non-ST segment elevation myocardial infarction (NSTEMI) ● ST segment elevation myocardial infarction (STEMI) 3. Distinguish among unstable angina (UA), non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI) in terms of pathophysiology, clinical manifestations (including ECG changes and serum cardiac markers) (p. 673-675).

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4 There are 2 key factors (diagnostics) that help distinguish between these disorders, ECG changes and serum biomarkers. Electrocardiogram (ECG) changes , i.e. T wave inversion, ST segment elevation, and Q wave. Changes vary depending on duration, extent, and location. To keep this simple, we’re focusing on ST segment elevation since that will tell you what kind of MI: NSTEMI vs. STEMI. The image to the right shows 1 heartbeat. ST segment elevation indicates myocardial ischemic injury (STEMI). In a 12 lead ECG, you can look at what lead (view of the heart) is showing ST segment elevation, which indicates what coronary artery is involved. If there is no ST segment elevation, but they have other signs of an MI (discussed next), that’s considered a NSTEMI. ST Elevation = STEMI If there is no ST elevation but blood draw shows patient is positive for serum biomarkers, then NSTEMI Serum biomarkers , i.e. cardiac-specific troponin I and troponin T and creatinine kinase MB (CK-MB). When myocardial cells become _ necrotic _, intracellular components are released into surrounding tissue, then picked up into blood circulation. These biomarkers are noted in a blood draw/lab work. Troponin rises within _ 3 _ hours and may remain elevated for how long? 7-10 days CK-MB rises within _ 4-8 _ hours and returns to normal when? 2-3 days Unstable angina and Non-ST-Segment Elevation MI Since UA and NSTEMI are on a continuum, they are presented under 1 heading in your text. Unstable angina Non-ST elevation MI ST elevation MI Pathophysiology 5 phases: 1. Unstable plaque ruptures or erodes with occlusive or nonocclusive thrombosis 2. Obstruction due to what? spasm, constriction, dysfunction, or adrenergic stimuli 3. Severe narrowing of the coronary lumen 4. Inflammation to occur 5. Physiologic state causing _ ischemia related to decreased oxygen supply _ (fever, hypotension) to the cardiac muscle Differences: in whether the ischemia is severe enough to cause sufficient enough damage to cause those serum biomarkers to be released Plaque disrupted with platelet aggregation + thrombus > occlusion . > then leads to Ischemic death of myocardial tissue. Principal biochemical consequence is conversion of aerobic metabolism to what? anaerobic metabolism with inadequate production of energy to sustain normal myocardial function Results in inadequate energy for normal myocardial fx. - Contractile f unction can be lost in 60 sec. - Ischemic area non-functioning within minutes - irreversible damage/necrosis in 20-40 min. Clinical Pain is persistent and severe and has at least Abrupt and severe chest pain , described

5 Unstable angina Non-ST elevation MI ST elevation MI manifestations 1 of 3 features: -occurs at rest or last more than 20 minutes -Severe pain of new onset -Pain is more severe or prolonged than previously experienced Is ST-segment elevated in either UA or NSTEMI? NO EK G changes, no ST segment elevation, normal levels Difference to note: UA: Positive or negative for serum biomarkers? NSTEMI: Positive or negative for serum biomarkers? as: abrupt, severe and crushing, often described as being constricting or suffocating . Located where? substernal region, radiating to the left arm, neck, or jaw, though it may be experienced in other chest areas Is it relieved by rest or nitroglycerin? NO What other manifestations may occur? -Females often experience atypical ischemic-type chest discomfort, whereas -the elderly may complain of shortness of breath more frequently than chest pain. -GI complaints are common, abdominal p ain, N/ V, indigestion, fatigue, weakness, tachycardia, anxiety, restlessness, sense of impending doom (like they'll die), cough with pink frothy sputum, pale or cool to the touch, hypotension, shock, death For a great visual overview, watch Khan Academy Diagnosing Myocardial Infarction (10:42) Next up: Chronic Ischemic Heart Disease Myocardial ischemia: blood flow through coronary arteries do not meet what? the metabolic demands of the heart. Most commonly the result of what? atherosclerosis What else may be involved? vasospasm 4. Describe the pathophysiology, precipitating factors, and clinical manifestations for chronic stable angina (p. 679). Pathophysiology: fixed coronary obstruction – blood does or does not meet the demands of the heart but not enough to cause necrosis to occur. What are some precipitating factors? increased demands of the heart, such as physical exertion, exposure to cold, and emotional stress. Winter time due to shoveling driveway, think its a heart attack but vessels aren’t constricting Clinical Manifestations Pain: describe characteristics and location: Pain is typically described as constricting , squeezing, or suffocating, steady pain. Commonly located in the precordial or substernal area of the ches t and may radiate to the left shoulder, jaw, arm, or other areas of the chest Usually provoked by exertion or emotional stress, relieved within minutes by what? rest or nitroglycerin Categorized as 1) occurs at rest, 2) new onset, and 3) increasing in intensity or duration.

6 Skim Cardiomyopathies if interested. On to Infectious Disorders. 5. Describe the etiology, pathophysiology and clinical manifestations of infective endocarditis and rheumatic heart disease (p. 685-687). Infective endocarditis Rheumatic heart disease Description Life-threatening infection of inner heart surface, heart valves and endocardium affected. Occurs with valvular issues, i.e. prolapse, prosthetic heart valves; implantable devices. Pacemakers and defibrillators Can develop into chronic valvular disorders that cause permanent dysfunction. Complication of an immune mediated response to group A Streptococcal throat infection. Can develop into chronic valvular disorder that can cause permanent dysfunction. Etiology Leading microbial cause is: Staphylococcal infections Streptococci and enterococci are other common causes. Major factor is seeding with what? bacteria Portal of entry may be obvious but can also be dental/surgical procedure. Streptococcal throat infection. Possible immunologic response. Pathogenesis Endothelial injury, bacteremia > fibrin- platelet thrombus along endothelial lining > bacteria seeding. Vegetative lesions form on valves: infectious organisms + cellular debris + fibrin strands > valve destruction. Immune mediated response to group A (beta-hemolytic) streptococcal (GAS) throat infection. Clinical manifestations Initially fever and signs of systemic infection , change in heart murmur, _ evidence of embolic _ distribution of vegetative lesions manifested as petechiae where ? Small petechial hemorrhages frequently result when emboli lodge in the small vessels of the skin, nail beds, and mucous membranes. Splinter hemorrhages under the nails of the fingers and toes are common Most have a hx of sore throat, headache, fever, abd pain, N/V, swollen glands, like strep throat Polyarthritis – affects one joint and moves to another Carditis that affects what? Can s ee inflammation in endocardium, myocardium, or pericardium SubQ nodules (nodules in wrist, elbow, ankle), erythema marginatum (lesions on trunk, upper arm, thigh), and Sydenham chorea (irritability, behavior problems, involuntary activities Resources Great review of Infective Endocarditis (4:01, stop at 3:25) Acute rheumatic fever & rheumatic heart disease (5:22, stop at 2:10)

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7 On to Valvular Heart Disease 6. Compare the effects of stenotic and regurgitant mitral and aortic valvular heart disease on hemodynamics and cardiovascular function (p. 688-693). Hemodynamic Derangements If needed, review pathway of blood flow through the heart (2:09). Function of the valve is to promote unidirectional blood flow through the heart. Dysfunction can result from what? Dysfunction of the heart valves can result from a number of disorders, including congenital defects, trauma, ischemic damage, degenerative changes, and inflammation. The most commonly affected valves are the mitral and aortic valves. Circle which valves are most commonly affected: Pulmonary Aortic Mitral Tricuspid Two types of mechanical disruptions occur with valvular heart disease: 1) Stenosis is _ narrowing _ of the valve orifice and failure of the _ valve leaflets _ to open normally. How does this affect the chamber emptying through the narrowed valve? The result in the chamber of the heart not emptying, increases the volume and workload o f the proceeding chamber. Significant narrowing of the valve orifice increases the resistance to blood flow through the valve, converting the normally smooth laminar flow to a less efficient turbulent flow . 2) Regurgitation (or an incompetent valve) occurs when the valve does not close properly , permitting _ backward _ flow of blood . How does this affect the chamber emptying through the regurgitant valve? flowing back into the LV during diastole when the aortic valve is affected and back into the left atrium during systole when the mitral valve is diseased. Th is increase the volume of the emptying chamber Skim the specific types if you want but manifestations common to most mitral and aortic valvular disorders (if progressed) are: ● Murmur heard with a stethoscope caused by turbulent blood flow through the valve . To hear a murmur (4:18, start at 1:05) ● Manifestations associated with left ventricular failure and pulmonary congestion: dyspnea, orthopnea, paroxysmal nocturnal dyspnea , fatigue Heart Failure At first glance, it seems odd that heart failure and circulatory shock are taught together but both reflect an impairment of the circulatory system resulting in the same compensatory mechanisms. Heart failure is a complex syndrome resulting from any function or structural disorder of the heart that results in manifestations of decreased cardiac output and/or pulmonary or systemic _ congestion _. We’ve already talked about several disorders that can cause heart failure. Can you list them here? To be able to apply your knowledge of pathophysiology to patients with heart failure, it’s important to know common hemodynamic terms. Let’s look back in the normal A&P chapter.

8 7. Define these hemodynamic terms: systole, diastole, stroke volume, ejection fraction, cardiac output, preload, afterload (p. 611-612, 614-615, 694). ● Systole: ventricular ejection (n ormal is 70 ml ~ 2.5 ounces) the period during which the ventricles are contracting ● Diastole – ventricular filling (normal is 110 ml ~ 4 ounces) the period during which the ventricles relax and fill with blood ● Stroke volume – amt. of blood ejected with each heartbeat. Difference between what? ● Ejection fraction (EF) – the fraction of the volume ejected at the end of diastole; stroke volume divided by _ end-diastolic volume _. Normal ex.: 70 divided by 110 = ~ _ 64 _% in a healthy person ● Cardiac output – amount of blood pumped each minute; product of what? product of stroke volume (SV) and heart rate (HR) (CO = SV × HR) ● _ preload _– end-diastolic pressure when the ventricle has been filled ● _ afterload _ – the work post contraction required to move blood into the aorta Pathophysiology. With heart failure, the CO does not meet the body’s demands. Heart failure is categorized as systolic vs. diastolic, and right vs. left ventricular dysfunction. 8. Differentiate between systolic dysfunction versus diastolic dysfunction and left ventricular versus right ventricular dysfunction (p. 695-697).

9 a. Systolic vs. diastolic: based on EF … what’s normal EF? about 55% to 70% 1) Systolic: ventricle cannot eject an adequate cardiac output; EF < _ 40 _ %. Does preload increase or decrease ? Where does blood accumulate? Atria and Venous system Caused by hypertension, STEMI, heart disease 2) Diastolic: EF is preserved but the left ventricle doesn’t fill adequately during diastole which reduces cardiac output. Causes: increased age, female gender, hypertension . Where does blood accumulate? Left Atria and P ulmonary Venous system b. Classified by ventricle affected: 1) Right: results in inability to move blood from systemic venous circulation to the pulmonary circulation. Where does blood accumulate? The v enous system Major effect: peripheral ___________. Remember learning about this earlier? Will see: Weight gain, edema, ascites (backs up into the GI system and liver), impaired

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10 liver function, JVD, anorexia (retaining fluid but because of GI symptoms causes toxins that affect appetite) Skinny but will have pitting edema Look at figure 27-22 and jot down the manifestations. 2) Left: impairs movement of blood from pulmonary circulation to arterial circulation which increases or decreases cardiac output. Accumulation of blood where? left ventricle, atrium, and pulmonary circulation Manifestations: decreased cardiac output = activity intolerance, decreased tissue perfusion, impaired gas exchange = cyanosis = signs of hypoxia Pulmonary edema = orthopnea cough with pink frothy sputum, difficulty breathing at night. Will need to sleep in a recliner or lots of pillow Look at figure 27-22 and jot down manifestations. Great review Khan Academy Heart Failure (8:36, stop at diagnosis) 9. Describe the compensatory mechanisms associated with heart failure (p. 697-699). Cardiac reserve is maintained due to compensatory mechanisms. Initially works great, then can be problematic. ● Frank-Sterling Mechanism: increase in end-diastolic volume (preload) > myocardial fibers stretch > increase force of contraction. In HF, decreased CO with reduced blood flow to kidneys > sodium and water retention. Can this be problematic in HF? Yes or No? Why? ● Sympathetic Nervous System (SNS): SNS stimulation occurs in response to decreased CO and SV. Heart rate and contractility, vascular tone regulation, renal sodium and water retention all increase. Can this be problematic in HF? Yes or No? Why? ● Renin-Angiotensin-Aldosterone Mechanism: Here are the steps ….. 1) Decreased cardiac output 2) Decreased renal blood flow and glomerular filtration rate 3) Sodium and water retention 4) Increased _ADH_ secretion by kidneys 5) Increased angiotensin II > vasoconstriction or vasodilation ? 6) ____________ is secreted that increases reabsorption of sodium and water 7) Antidiuretic hormone is increased which causes what? YIKES! How is this an issue in HF?

11 ● Natriuretic peptides are produced and secreted by the heart muscle: these peptides have what kind of an action? ● Myocardial hypertrophy and remodeling: changes structure and function > pump dysfunction and hemodynamic overload. Not good in HF. Before we move on, take a look at figure 27-24 on p. 698. Can you see how these compensatory mechanisms can be a problem for a patient with HF? Skim info about Acute Heart Failure Syndrome (very scary!). 10. Describe the clinical manifestations and underlying pathophysiologic mechanisms of heart failure (p. 700-701). Manifestations depend on extent and type of dysfunction. A person fairly stable may decompensate quickly. What is a frequent cause? A. Respiratory Manifestations: due to congestion of what? Define these terms: 1) Dyspnea - SOB 2) Exertional dyspnea - Perceived SOB when related to increased activity 3) Orthopnea - shortness of breath occurring when supine 4) Paroxysmal nocturnal dyspnea - sudden attack of dyspnea during sleep 5) Cheyne Stokes respiration - a pattern of periodic breathing characterized by gradual increase in depth (and sometimes rate) of breathing to a maximum, followed by a decrease resulting in apnea 6) Acute pulmonary edema (0:56): capillary fluid moves into alveoli – life threatening! Describe what these patients look like: seen sitting and gasping for air. Pulse is rapid, skin is moist and cool, and lips and nail beds are cyanotic. As the pulmonary edema worsens and oxygen to the brain drops, confusion and stupor appear. B. Fatigue, Weakness, and Mental Confusion due to decreased CO. C. Fluid retention and edema: many manifestations are due to increased hydrostatic (capillary) pressure (remember this from fluid and electrolytes? Hope so.) . Define this terms: 1) Nocturia: a nightly increase in urine output that occurs relatively early in the course of heart failure. 2) Oliguria: a decrease in urine output, is a late sign related to a severely reduced CO and resultant renal failure. D. Cardiac cachexia and Malnutrition: What causes this? people with end-stage heart failure. Factors contributing to its development may include fatigue and depression that interfere with food intake, congestion of the liver and GI structures that impairs digestion and

12 absorption and produces feelings of fullness, and circulating toxins and mediators released from poorly perfused tissues that impair appetite and contribute to tissue wasting. E. Cyanosis: bluish discoloration of skin and mucous membranes is caused by what? excess desaturated hemoglobin in the blood F. Arrhythmias and Sudden Cardiac Death: due to interruption of normal electrophysiology of heart caused by altered structure and hypoxemia Super summary: Understanding HF (1:46). Patient perspective on HF (3:16) Time to jump to our last topic: Circulatory Failure (Shock) 11. Define circulatory shock and describe the pathophysiology/compensatory mechanisms (p. 718- 720). Circulatory shock is an acute failure of the circulatory system to do what? to supply the peripheral tissues and organs of the body with an adequate blood supply, resulting in cellular hypoxia. Shock is a syndrome that can occur in many traumatic conditions or disease states. Pathophysiology Most immediate compensatory mechanisms are Compensatory Mechanisms Effect Sympathetic nervous system: plays an important role in the compensatory response to decreased CO and SV. It initially helps maintain perfusion of the body organs Blood vessels: Vasoconstriction or vasodilation? Heart rate: increased Myocardial muscle: volume increases length Bronchioles: Relaxation Renin release Results in what? increase in angiotensin II, which augments vasoconstriction and leads to an aldosterone-mediated increase in sodium and water retention by the kidneys. NOTE: These mechanisms are not effective over the long term and become detrimental. Let’s look at the different types. 12. Compare the etiology, pathophysiology and clinical manifestations of cardiogenic, hypovolemic, distributive (neurogenic, anaphylactic, and septic), and obstructive shock (p. 720-726). Type of Shock Etiology/Pathophysiology Clinical Manifestations Cardiogenic Heart fails to pump blood sufficiently to meet the body’s demands. What’s the most common cause? MI List: hypoperfusion with hypotension, although a preshock state of hypoperfusion may occur with a normal

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13 Type of Shock Etiology/Pathophysiology Clinical Manifestations Dec. CO and SV leading to compensatory mechanisms like HF. Eventually coronary artery perfusion is impaired. blood pressure. The lips, nail beds, and skin may become cyanotic because of stagnation of blood flow and increased extraction of oxygen from the hemoglobin as it passes through the capillary bed. Decreased perfusion. Mean arterial and systolic blood pressures decrease because of poor SV, and there is a narrow pulse pressure and near-normal diastolic blood pressure because of arterial vasoconstriction. Urine output decreases because of lower renal perfusion pressures and increased release of aldosterone. Elevated preload is reflected in a rise in CVP and PCWP. Neurologic changes, such as alterations in cognition or consciousness, may occur because of low CO and poor cerebral perfusion. Death Hypovolemic Acute loss of _ 15-20 _% of circulating blood volume Caused by loss of whole blood, internal hemorrhage, third-space losses Compensatory mechanisms kick in. See figure 27-37. Manifestations are due to compensatory mechanisms. List here and circle the early signs/symptoms. Tachycardia, Vasoconstriction, increase thirst As shock progresses: can have weak thready pulse, decreased BP, rapid respirations, decreased urine output, restlessness, agitation, LOC, coma, death Distributive (3 types) Loss of blood vessel tone, enlargement of the peripheral vascular compartment, displacement of vascular volume away from the heart and central circulation. Blood volume is NORMAL. Neurogenic shock : caused by what? decreased sympathetic control of blood vessel tone resulting from a defect in the vasomotor center in the brain stem or the sympathetic outflow to the blood vessels Examples? Spinal shock, anesthesia, drug over dose Anaphylactic shock : most severe systemic List the manifestations of the 3 types here. Highlight how they differ. thirst, increased HR, cool and clammy skin, decreased arterial blood pressure, decreased urine output, and changes in mentation. Anaphylactic shock manifestations: apprehension, abdominal cramps, hives, itching, warm burning sensation, choking,

14 Type of Shock Etiology/Pathophysiology Clinical Manifestations allergic reaction. Examples? Anaphylactic hypersensitivity 1 Septic : most common type of distributive (vasodilatory) shock; systemic immune response to severe infection; release of proinflammatory and anti-inflammatory mediators, endothelial dysfunction which alters coagulation. Check on figure 27-38 on p. 725. coughing Septic shock: Hypotension, warm flushed skin, decreased blood volume, fever, increased wbc, decreased urine output Sepsis = look for that immune response or it doesn't reach organ failure Obstructive Results from mechanical obstruction of blood flow in central circulation. What are some causes? Circle the most common. dissecting aortic aneurysm, cardiac tamponade, pneumothorax, atrial myxoma, and evisceration of abdominal contents into the thoracic cavity because of a ruptured hemidiaphragm. The most frequent cause of obstructive shock is PE or DVT*** Elevated right heart pressure because of impaired right ventricular function. Signs of right ventricular heart failure, such as elevated central venous pressure and jugular venous distention. To keep shocks straight, check out this video: Shock on Khan Academy (9:46). A little more detail than you need but still helpful. Skim the complications of shock. These are addressed elsewhere but remember shock may be the cause. Reference: Norris, T. L. (2020). Porth’s Essentials of Pathophysiology, 5th edition. Wolters Kluwer. Menti Which has ST segment elevation on EKG, elevated Troponin I and T and CK-MB? STEMI Which has chest pain (angina) brought on by exertion and is relieved by rest? Chronic Stable Angina Which has no ST segment elevation, troponin I and T and CK-MB are elevated? NSTEMI Which has severe crushing chest pain, radiating to left shoulder, not relieved by rest or nitroglycerin, N/V, and impeding doom? STEMI

15 Which has chest pain increasing in severity, duration and frequency, no other symptoms or diagnostics? Unstable Angina

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SG F21 Disorders Cardiac Function, Heart Failure, Circulatory Shock

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