Case 2 SLOs

Differentiate between angina and chest pain. Angina-pain Chest pain-mostly commonly referred pain to a cardiac anomaly right over the sternal border Differentiate between stable, unstable and variant angina. Stable angina-the pain is predictable and present only during exertion or extreme emotional distress, and it disappears with rest. Usually secondary to atherosclerosis; exertional chest pain in classic distribution (usually with ST depression on ECG), resolving with rest. Unstable angina-this may signal an impending heart attack. Unstable angina is angina pain that is different from your regular angina pain or pain that occurs while at rest. The angina may occur more frequently, more easily at rest, feel more severe, last longer, or come on with minimal activity. Thrombosis with incomplete coronary artery occlusion; ST depression on ECG (increase in frequency or intensity of chest pain; any chest pain at rest). Prinzmetal's (Variant) angina-this is when angina occurs at rest, when sleeping, or when exposed to cold temperatures. In these cases, the symptoms are caused by decreased blood flow to the heart muscle from a spasm of the coronary artery. The majority of people with this type of angina also have coronary artery disease. These spasms occur close to the blockage. Occurs at rest secondary to coronary artery spasm; transient ST elevation on ECG. Known triggers include tobacco, cocaine, and triptans, but trigger is often unknown. Treat with calcium channel blockers, nitrates, and smoking cessation.

Define diaphoresis, and explain the role of the autonomic nervous system in mediating this response, and the unique nature of the post-ganglionic adrenergic afferents involved. Diaphoresis-sweating ANS involvement- Sweat glands only receive sympathetic innervation from postganglionic fibers via muscarinic acetylcholine receptors. This leads to the activation of phospholipase C, which, in turn, stimulates protein kinase C and raises Ca2+. These signals somehow trigger the primary secretion, which follows the general mechanism for Cl secretion.

Define silent ischemia, and explain why it is believed to be more commonly described among diabetic patients. Silent ischemia-ischemia (restriction of blood flow and subsequent oxygen supply to an area) without pain Patients with silent ischemia are more commonly believed to be among diabetic patients because they are affected by diabetic neuropathy. Additionally, a previous MI can put one at risk for silent ischemia and patients may have an MI with no prior warning.

Provide an overview of Lisinopril, focusing on the mechanism of action of this drug. ACE inhibitor that is used to decrease blood volume and thus decrease blood pressure by inhibiting the angiotensin II receptor in renin angiotensin system (which would normally increase BP)

Explain the significance tachycardia in the presence of marked hypotension, and interpret this with respect to the status of the cardiovascular system. The heart is compensating for decreased preload and/or ejection fraction. This means the system is struggling and indicates a system of cardiogenic shock.

Explain the value of jugular venous pressure in assessing the status of the cardiovascular system. In doing so, provide normal values for venous pressure, and potential causes of elevated venous pressure. Low JVP indicates hypovolemia while high JVP indicates cardiogenic or obstructive shock. Normal JVP level: 6-8 cm of H20 Elevated venous pressure can be caused by left sided or right sided heart failure. Left sided backs up into pulmonary circuit backing up into right ventricle and ultimately causes high JVP.

Explain how cardiac insufficiency can lead to increased jugular venous pressure, and therefore pulmonary edema. Also predict the effect of this on lung V/Q ratio. The JVP is raised in right-sided heart failure. Chronic hypoxia in COPD leads to pulmonary arterial vasoconstriction, pulmonary hypertension, right heart dilatation and peripheral edema with elevation of the JVP. The V/Q ratio will be high, because there will be decreased perfusion.

Describe the effect of anterior wall myocardial ischemia and infarct on the normal ECG with respect to the ST-segment of the trace, and which leads normally express this pathologic marker. State the therapeutic benefits of morphine, dobutamine and dopamine in treatment of cardiac insufficiency following infarct; include the mechanism through which they exert cardiovascular benefit. Morphine- decreases the pain-induced release of catecholamines that cause further vasoconstriction and worsen MI. Dobutamine- Beta adrenergic agonist that increases heart contractility. Dopamine- Beta 1 and alpha 1 agonist, is going to cause vasoconstriction and stronger and faster contractions. Summarize the benefit of an intra-aortic balloon pump with respect to coronary blood flow and left ventricular afterload, and explain the mechanical principles by which why these benefits occur. The balloon blows open the blocked artery allowing for blood flow. The expanded stent remains in place after the deflated balloon is withdrawn. This would improve contractility by returning blood flow to the tissue and thus help to decrease the left ventricular afterload

Define cardiogenic shock. Heart is unable to deliver enough blood to maintain adequate tissue perfusion, hypotension combined with signs of poor tissue perfusion, vasoconstriction, high JVP, and cool extremities, all in the setting of myocardial dysfunction. Low cardiac output and high SVR due to myocardial pump failure. Generally see crackles and pulmonary edema. Causes: this can be due to intrinsic myocardial damage (infarction), ventricular arrhythmias, extrinsic compression, and pump failure.

Differentiate between cardiogenic shock and hypovolemic shock in terms of the mechanism of cardiovascular dysfunction. Cardiogenic shock - Cardiogenic shock occurs when there is pump failure. Clinically, patient will present cold to the touch, increased jugular venous pressure, and with lung sounds on auscultation (due to heart failure and pulmonary edema). Pump failure from:1. Arrhythmias1. Valve dysfunction 1. Cardiomyopathies The common factor is that they all filter into DECREASED cardiac output.

Hypovolemic shock - Condition in which severe blood or fluid loss leads to decreased cardiac output and decreased tissue perfusion. Clinically, patient will present with cold extremities, and decreased jugular venous pressure. Decreased volume from:1. Trauma (severe burn)1. Dehydration 1. Hemorrhage Common factor is that they all lead to loss of circulating blood volume which causes decreased venous return and thus decreased cardiac output.

Explain the mechanistic basis of cardiogenic shock secondary to three common causes; this explanation should include the effects on SV, CO, autonomic tone, systemic vascular resistance, blood pressure, and tissue blood flow. Suggested causes may include: myocardial infarct, acute severe aortic regurgitation, pericardial tamponade. Myocardial infarction-pump not functioning. Cardiogenic shock is generally associated with the loss of more than 40% of the left ventricular myocardial muscle. Progressive myocardial necrosis with infarct extension. Decreased coronary perfusion pressure and increased myocardial oxygen demand. Limited coronary blood flow reserve. Mechanical defect where ventricle is able to eject less volume per beat (decreased SV and CO). Attempt to enhance cardiac output by this mechanism comes at the cost of having a higher left ventricular diastolic filling pressure, which ultimately increases myocardial oxygen demand and causes pulmonary edema. As a result of decreased contractility, the patient develops elevated left and right ventricular filling pressures and low cardiac output. Overall, decreased SV resulting in decreased CO, increased systemic vascular resistance causing decreased blood flow to many tissues, and hypotension. Acute severe aortic regurgitation- unadapted ventricle is subjected to a sudden increase in volume. This increase in volume leads to a precipitous increase in left ventricular diastolic pressure. The pressure may exceed that of the left atrium, prematurely closing the mitral valve, and it may then increase to equilibrate with aortic diastolic pressures, limiting further regurgitation and opening the aortic valve in diastole. The forward stroke volume decreases and cardiac output is maintained through compensatory tachycardia. Pericardial tamponade-pericardial effusion where blood/fluid accumulates in the pericardium. Marked reduction in diastolic filling, which results when transmural distending pressures become insufficient to overcome increased intrapericardial pressures. Tachycardia is the initial cardiac response. Heart is compressed throughout the cardiac cycle, systemic venous return is impaired and right atrial and right ventricular collapse occurs. Blood preferentially accumulates in the venous circulation, at the expense of LV filling. This results in reduced cardiac output and venous return. Overall, decreased SV resulting in decreased CO, increased systemic vascular resistance causing decreased blood flow to many tissues, and hypotension

Provide a brief overview of the epidemiological aspects of cardiogenic shock (CS); Include the incidence among patient suffering from acute myocardial infarct, the most common causes of CS, in hospital mortality rates, and the effects of age, diabetes, and anterior wall infarcts on risk of developing CS. Incidence among patient suffering from acute myocardial infarct: Early shock, defined as occurring in less than 24 hours, was found in 74% of patients in a recent study. The most common causes of CS: Left ventricular dysfunction (LVD) is the most frequent cause of cardiogenic shock (acute MI), main etiology 75% pts. [This was followed by acute mitral regurgitation (8.3%), ventricular septal rupture (4.6%), isolated right ventricular shock (3.4%), tamponade or cardiac rupture (1.7%), and other causes (8%)]. In hospital mortality rates: Despite emerging innovative treatments, in-hospital mortality in patients with cardiogenic shock continues to be as high as 70-80%. Other studies have quoted mortality rates of around 50% to 80%. With effective and newer treatments and techniques some studies have mortality rates dipping below 50%. Effects of age: being elderly predispose patients with myocardial infarction to develop shock. Effect of diabetes: Diabetics are twice as likely to develop cardiogenic shock as non-diabetics with AMI. However, the prognosis of cardiogenic shock is similar in both groups of patients. The mechanisms of diabetes affecting CS are largely unknown but thoughts are that abnormal glucose metabolism causes macrovascular damaging, complicating AMI. Anterior wall infarcts on risk of developing CS: Infarctions were located anteriorly in most of the patients (55%) in the SHOCK trial registry. The left anterior descending artery (LAD) was found to be the most frequently involved artery unrelated to the time of shock onset.

**Perfusion and no ventilation is a shunt so V/Q is decreased. If you have ventilation and no perfusion, it is considered to be dead space so V/Q increases.**

Define the term cardiac index, and differentiate between this and cardiac output; also describe the Fick principle for determining cardiac output, and the nature of the measurements involved. is better than CO alone because relates to size of individual

Fick PrincipleCardiac output can be measured by knowing arterial and mixed venous O2 content AND oxygen consumptionOxygen consumption(VO2), is the amount of oxygen extracted from respired air at the lung and is equivalent to the oxygen consumed in the body tissues. It can be calculated by multiplying VE by the change in the partial pressure of oxygen in inspired vs. mixed expired air VO2, oxygen consumption in ml of pure gaseous oxygen per minute. This may be measured using a spirometer within a closed rebreathing circuit incorporating a CO2absorber Ca, the oxygen concentration of blood taken from the pulmonary vein (representing oxygenated blood) Cv, the oxygen concentration of blood from an intravenous cannula (representing deoxygenated blood)Define pulmonary capillary wedge pressure (PCWP), and explain how it is determined; further, explain the relationship between pulmonary capillary wedge pressure, left atrial pressure, and left ventricular pressure. PCWP is a measure of the left atrial pressure and is measured by inserting a pressure tip through the lateral cubital vein and feeding the system into the pulmonary artery. Normal value is 8-10 mmHg. PCWP is a good estimate of left ventricular pressure during diastole

Define the term preload as this applies to the ventricles, and provide an overview of the determinants of ventricular preload; then explain how an increase or decrease in preload affects cardiac output, and by what mechanism. Preload is the ventricular refill during diastole that is determined by venous return and ventricular compliance. Increase in preload will cause an increase in CO while a decrease will cause the opposite to happen.

Differentiate between volume-responsive shock and shock which is refractory to expanding vascular volume. Volume-responsive shock-hypovolemia cases where not enough circulating volume and not enough tissue perfusion. Shock refractory to expanding vascular volume-the heart is full even though the CO is low, thus adding more fluid wouldnt help to increase CO because the pump is not functioning properly-it would just result in backing up into the lungs further

Define the term inotrope, and explain the cellular basis for inotropic effects. An inotropic drug is a medicine that alters the force or strength of the heart's muscular contractions (heartbeats). There are two different types of inotropic drugs: negative and positive. Negative inotropic drugs make the heart beat less strongly, and positive inotropic drugs make the heart beat more strongly Calcium plays an important role in the process of heart muscle contraction. In general, calcium levels are increased by positive inotropic drugs and decreased by negative inotropic drugs.

Define the term chronotropic effect, and explain why a positive chronotropic effect is not typically advantageous in the setting of cardiogenic shock. Affects the rate of the contraction (HR) where positive chronotropes increase the HR while negative chronotropes decrease the HR. Chronotropic effect not advantageous in the state of cardiogenic shock because the patient already has an elevated HR, but the heart is not pumping effectively, so adding to this problem by increasing the HR would not facilitate improved CO.

Describe what is meant by a percutaneous left ventricular assist device.

Define the term afterload as this applies to the cardiovascular system. Explain what the significance of afterload is for cardiac output, and cardiac work. Following from this, explain what unloading the left ventricle means, and why this strategy can improve outcomes in management of severe cardiogenic shock. Afterload is the pressure against which the heart must work to eject blood during systole (systolic pressure). Increase in afterload will cause a decrease in CO and an increase in cardiac work. Unloading the left ventricle refers to decrease afterload w either decreased resistance or decrease afterload using a pLVAD. Preload is unaffected since the pLVAD works during systole.

Define atrial fibrillation and ventricular fibrillation, and explain which has a worse acute prognosis and why this is the case based upon the function of the chambers affected.**Ventricular fibrillation is worse**Atrial fibrillation-quivering or irregular heartbeat (arrhythmia) that can lead to blood clots, stroke, heart failure and other heart-related complications. Even when AF isn't noticed, it can increase the risk ofstroke.

Ventricular fibrillation- is the most serious cardiac rhythm disturbance. The lower chambers quiver and the heart can't pump any blood, causing cardiac arrest.