Pathophysiology Exam 2 Study Guide (PDF)

CARDIOVASCULAR SYSTEM DISEASES OF THE ARTERIES: HYPERTENSION - Consistent elevation of systemic arterial blood pressure - Sustained systolic (when your heart contracts, pushes the blood out) blood pressure of 130 mmHg or greater - Diastolic pressure (when hea...

CARDIOVASCULAR SYSTEM DISEASES OF THE ARTERIES: HYPERTENSION - Consistent elevation of systemic arterial blood pressure - Sustained systolic (when your heart contracts, pushes the blood out) blood pressure of 130 mmHg or greater - Diastolic pressure (when heart is at rest between beats; refilling of the blood) of 80 mmHg or greater - Types - Primary (essential) hypertension (95%)- genetic and environmental factors - like diet, stress, and lifestyle; No specific disease is the cause. - Genetic predisposition to hypertension is thought to be polygenic and associated with epigenetic changes influenced by diet and lifestyle. - Secondary hypertension (5%) caused by an underlying primary disease or drugs - Signs/symptoms are seen as something else - happens because of another disease (like kidney problems) or from taking certain medications. - Most significant factor in causing target organ damage PRIMARY (ESSENTIAL) HYPERTENSION - Blood pressure consistently above 140/90 mm Hg Pathophysiology - Increase in arteriolar vasoconstriction → increase total peripheral resistance (also known as systemic vascular resistance (SVR) is the force exerted on blood by the body's blood vessels)→ elevated blood pressure - AKA; The blood vessels tighten → this makes it harder for blood to flow → which increases blood pressure. - the small blood vessels (arterioles) get narrower (vasoconstriction). When this happens, it’s harder for blood to flow through them, creating more resistance in the blood vessels. This makes the heart work harder to push the blood through, which raises your overall blood pressure. - Overactivity of the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS), and alterations in natriuretic peptides - The SNS is responsible for the body’s "fight or flight" response, which increases heart rate and tightens blood vessels when needed. - In hypertension, the SNS becomes overactive, leading to: - Increased heart rate and Vasoconstriction - The RAAS thinks the blood pressure is low even when it’s not: holds onto water and sodium - Natriuretic peptides - Hormones produced by the heart: They work by causing vasodilation (widening of blood vessels) and promoting the excretion of sodium and water by the kidneys, which lowers blood volume and blood pressure.  - In hypertension, the effectiveness of these peptides may be reduced or altered, meaning they do not adequately counteract the high blood pressure and fluid retention caused by the SNS and RAAS. This contributes to the persistence of high blood pressure. - Increased vascular volume is related to a decrease in renal excretion of salt hence the shift in pressure natriuresis relationship - For any given blood pressure, individuals with hypertension tend to secrete less salt in their urine - Inflammation, endothelial dysfunction, obesity related hormones, and insulin resistance - Over time → damage to arterial walls - Blood supply is reduced → ischemia and necrosis of tissues Obesity, hypertension, dyslipidemia, and glucose intolerance often are found together in a condition called the metabolic syndrome NON-MODIFIABLE - Positive family history - The older you age the blood vessels harden = high blood pressure - Advancing age - Sex - Males > females - males : middle age; females (older, 65+) - Race: black - More prone to hypertension MODIFIABLE - High sodium intake - Glucose intolerance (diabetes mellitus)/insulin resistance - individuals can make lifestyle changes—such as improving their diet, increasing physical activity, and managing weight—to lower their blood glucose levels, improve insulin sensitivity, and consequently reduce their risk of developing or worsening hypertension. - Obesity - Heavy alcohol use - Cigarettes - Inflammation - Damage of blood vessels can make them more prone to stiffness and thickening - Linked to SNS and RAAS - Dyslipidemia: high cholesterol  - High levels of LDL (bad cholesterol) can lead to a buildup of plaque in the arteries Clinical presentation: asymptomatic (silent disease) Baseline assessment - Complete blood count (CBC) and kidney panel (bun and creatinine) - Urinalysis - Lipid profile - blood test that measures the levels of various types of lipids (fats) in your bloodstream - Electrocardiogram (EKG)- electrical activities of the heart - Echocardiogram- imaging of the heart (ultrasound) TREATMENT - Lifestyle: reduce risk - Low sodium diet - DASH diet - Dietary Approaches to Stop Hypertension (DASH) diet is a healthy eating plan that focuses on vegetables, fruits, and whole grains, and limits foods high in salt, saturated fat, and sugar. - Exercise - Weight reduction - Decrease stress - Alcohol moderation - Education - Medical: pharmacological - Diuretic → water - help the body eliminate excess sodium (salt) and water through the urine. - Angiotensin converting enzyme inhibitors (ACE- inhibitors) - prevent the conversion of angiotensin I to angiotensin II, a powerful vasoconstrictor. By blocking this conversion, ACE inhibitors help relax blood vessels, reducing blood pressure - Angiotensin-II receptor blockers (ARB) - block the action of angiotensin II by preventing it from binding to its receptors on blood vessels. This helps the blood vessels stay relaxed and open, leading to lower blood pressure. STANDARD ^^^^^^ - Calcium channel blockers - By reducing calcium's effect, the blood vessels relax, and the heart doesn't have to pump as hard, which lowers blood pressure. - Aldosterone antagonists  - block the effects of aldosterone, a hormone that causes the body to retain sodium and water. By blocking aldosterone, these medications help reduce fluid buildup in the body and lower blood pressure. - Beta blockers - blocking the effects of adrenaline (epinephrine) on beta receptors in the heart. This action slows the heart rate and reduces the force of contraction, which decreases the amount of blood pumped and lowers blood pressure. COMPLICATIONS Malignant hypertension - Also known as - Hypertensive crisis - Resistant hypertension - Sudden and rapid increase in arterial blood pressure - Systolic pressure usually > 180 mmHG - Diastolic pressure is usually > 140 mmHG - Life threatening with end organ damages (Or long term complications) SECONDARY HYPERTENSION Caused by a systemic diseases that raises peripheral vascular resistance and or cardiac output - A medical condition affects the blood vessels (raising resistance to blood flow) or the heart's pumping ability (increasing the amount of blood being pushed out). - Specific identifiable pathology or condition - high blood pressure that results from other health problems that either make it hard for blood to flow or make the heart work harder to pump blood Question: How does this differ from primary hypertension? - Primary hypertension develops on its own without a specific cause, while secondary hypertension is caused by another health issue that affects blood pressure. - Treat underlying problems to reduce blood pressure - BP normalized after treatment - Congenital (present at birth) or manifest later in like PROGRESSION - Endothelial injury and inflammation - Injury to the endothelium can trigger an inflammatory response in the blood vessel walls, leading to further damage and dysfunction - Cellular proliferation  - In response to injury and inflammation, smooth muscle cells in the blood vessel walls begin to proliferate (multiply). This process can lead to thickening of the vessel wall and reduced lumen size, increasing vascular resistance. - Macrophage migration - Macrophages are a type of white blood cell involved in the immune response. They migrate to the site of endothelial injury to engulf and digest cellular debris and oxidized LDL cholesterol. - Their presence also contributes to the inflammatory process, releasing substances that can further damage blood vessel walls - Low density lipoproteins (LDL) oxidation (foam cell formation) with oxidative stress - LDL cholesterol is often referred to as "bad" cholesterol. When LDL particles become oxidized in the bloodstream, they trigger inflammatory responses. - Macrophages ingest oxidized LDL and transform into foam cells. The accumulation of foam cells contributes to the formation of fatty streaks in the arterial walls, a precursor to atherosclerosis. - Fatty streak - early stage of atherosclerosis. It consists of lipid-laden foam cells that accumulate within the arterial walls, signaling the beginning of plaque formation. - Fibrinous plaque - fatty streaks can develop into more advanced fibrinous plaques. These plaques contain not only lipids but also proteins, such as fibrin, which contributes to clot formation and further narrows the artery. - Complicated plaque - additional inflammatory cells, necrotic (dead) tissue, and calcification. Complicated plaques are more unstable and more likely to rupture. - Result - ischemia → necrosis - The narrowing of the arteries caused by plaque formation reduces blood flow, leading to ischemia, a condition where there isn’t enough blood (and therefore oxygen) reaching tissues. - If ischemia is severe or prolonged, it can result in necrosis, which is the death of tissue due to lack of blood supply. This can affect vital organs, leading to complications like heart attacks or strokes. CORONARY ARTERY DISEASE - Any vascular disorder that narrows or occludes the coronary arteries leading to myocardial ischemia → myocardial infarct - The narrowing or blockage usually happens because of plaque buildup (made of fat, cholesterol, and other substances) in the arteries. This process is called atherosclerosis. - When the arteries narrow, less blood can flow to the heart muscle. - Myocardial ischemia: This means that the heart muscle isn’t getting enough oxygen-rich blood.  - Myocardial infarction: If the blood flow is severely reduced or blocked completely, it can lead to a heart attack, where part of the heart muscle dies due to lack of blood and oxygen. - Etiology - Atherosclerosis (most common cause) - Aka: ischemic heart disease, coronary heart disease NONMODIFIABLE - Genetic abnormalities - Family history - Increasing age - Male gender - Female gender (postmenopausal) MODIFIABLE - Hyperlipidemia - high levels of fats in the blood, which can increase the risk of serious health issues like heart disease and stroke. It can often be managed with lifestyle changes and, when necessary, medications. - Hypertension - Cigarette smoking - Diabetes - Inflammation - Obesity - Sedentary lifestyle ANGINA PECTORIS = CHEST PAIN Myocardial ischemia leads to angina pectoris = chest pain Pathogenesis - Transient, local, temporary deprivation of the coronary blood supply that cannot meet the demand of the myocardium for oxygen and nutrients Types - Blockage (thrombus, embolus) - stable/classic/ exertional angina pectoris - Unstable angina pectoris - Spasms → prinzmetal (variant) angina CLASSIC/STABLE ANGINA PECTORIS - transient substernal chest pain - medical term that describes a temporary discomfort or pain located in the center of the chest, just behind the breastbone. The word "transient" means that the pain is short-lived and doesn't last for a long time. - Pressure, heaviness, squeezing, burning, or choking sensation - Pallor, diaphoresis (Excessive sweating), nausea - Triggered by physical or emotional distress - Short lasting (1-5 minutes) - Relieved with rest and/or nitroglycerine - Severity of chest pain and duration of symptoms- an indication of disease progression - Physical exam/assessment- often normal Medications: - Nitrate (nitroglycerin) - Nitroglycerin is a vasodilator that relieves angina by widening blood vessels, which increases blood flow to the heart and reduces the heart's workload - Beta blockers - Beta blockers slow down the heart rate and reduce the force with which the heart contracts. - Calcium channel blockers - relax the heart muscle and dilate blood vessels. - Similar to nitrates, calcium channel blockers increase blood flow to the heart and reduce chest pain. When the heart muscles (myocardium) relax, particularly in response to medications like calcium channel blockers or nitrates, the smooth muscle in the blood vessel walls also relaxes. This relaxation leads to vasodilation, or widening of the blood vessels, which decreases vascular resistance - statins - lower cholesterol levels in the blood. - By reducing cholesterol levels, statins can help to slow down the progression of atherosclerosis, a condition that narrows the arteries and can lead to angina. - Ranolazine-antianginal - blocking sodium channels in the heart, which helps to reduce the heart's workload and improve blood flow ACUTE CORONARY SYNDROME - Sudden coronary obstruction - This means that a blockage occurs suddenly in the coronary arteries. - Thrombosis formation over a ruptured atherosclerotic plaque - plaque (made of fat, cholesterol, and other substances) in the arteries can rupture, leading to the formation of a blood clot (thrombus) over it, which can block blood flow. - Embolus - A blood clot or debris that can travel and cause a blockage in a smaller artery.  - Clinical presentation - Unstable angina: reversible myocardial ischemia (tissue injury) - Myocardial infarction - Sudden and extended obstruction of blood flow - Irreversible myocardial cell death UNSTABLE ANGINA PECTORIS - Reversible myocardial ischemia without detectable myocardial necrosis - Lack of oxygen to the heart muscle is temporary and can be reversed, meaning no permanent damage to the heart tissue occurs. - "Necrosis" refers to tissue death. In unstable angina, although there is reduced blood flow to the heart, it has not yet caused the death of heart muscle cells (which would indicate a heart attack) - - Thrombotic or embolic events with reperfusion before necrosis - AKA: A blood clot blocks blood flow, but blood starts flowing again before any permanent damage or cell death occurs - BREAKDOWN: - A thrombus is a blood clot that forms in a blood vessel, while an embolus is a clot that travels through the bloodstream. These events can block or reduce blood flow to the heart. - Reperfusion" is the restoration of blood flow to an area that was previously ischemic. In unstable angina, blood flow is restored before necrosis (cell death) can occur, which is why the ischemia is reversible. - Foreshadowing an impending infarction - warning sign of a potential heart attack (myocardial infarction) in the near future. - Clinical presentation - Angina at rest - chest pain or discomfort occurs even when you are not doing any physical activity. Normally, angina is triggered by exertion, but in unstable angina, the pain can happen even when you're resting. - Longer duration and lower in threshold (easier to trigger chest pain) - takes less exertion to trigger the pain. For example, it might happen during minimal activity or stress, whereas stable angina usually requires more intense activity (like exercise) to cause pain - Does not respond to nitroglycerine - Nitroglycerine is a medication commonly used to relieve chest pain by opening up the blood vessels to improve blood flow to the heart. In stable angina, nitroglycerine often helps. However, in unstable angina, chest pain does not go away with nitroglycerine, making it more serious and requiring immediate medical attention. Coronary Artery Disease (CAD) CAD occurs when the coronary arteries (which supply oxygen-rich blood to the heart muscle) become narrowed or blocked, usually due to a buildup of plaque (a mix of fat, cholesterol, and other substances). This process is called atherosclerosis.  The narrowed arteries restrict blood flow, which reduces the supply of oxygen to the heart, especially when the heart is working harder (during exercise or stress). How Angina Relates to CAD 1. Stable Angina and CAD: ○ In stable angina, there is a partial blockage in the coronary arteries caused by CAD. The reduced blood flow cannot meet the heart's increased oxygen demand during physical activity or stress. ○ The chest pain occurs when the heart is temporarily starved of oxygen, but this can be managed by resting or using medications like nitroglycerine, which improves blood flow. 2. Unstable Angina and CAD: ○ Unstable angina is a more serious condition and often a direct result of CAD worsening. A plaque rupture or blood clot can form on top of the narrowed artery, severely restricting blood flow. ○ This type of angina can happen at rest, last longer, and signals that a heart attack (complete blockage and damage to heart tissue) may be imminent if the blockage isn't treated. 3. Prinzmetal's (Variant) Angina and CAD: ○ While Prinzmetal’s angina is not directly caused by atherosclerosis, it can occur in people with or without CAD. In this type, a spasm in the coronary arteries temporarily restricts blood flow, even in arteries that may not have significant plaque buildup. Summary of the Relationship: CAD is the underlying cause of most cases of angina, as the narrowed arteries limit oxygen-rich blood flow to the heart. Stable angina is a predictable symptom of CAD, triggered when the heart's oxygen demand increases. Unstable angina is a more dangerous sign of CAD, often indicating that a blood clot or significant plaque rupture is blocking the artery, potentially leading to a heart attack. Prinzmetal's angina can occur independently of CAD but may still be seen in individuals with coronary artery disease. Angina is essentially a symptom of the reduced blood flow caused by CAD, with unstable angina being an indicator of more severe disease progression. Myocardial infarction - Prolonged lack of oxygen supply (ischemia) → leads to irreversible damage to the heart muscle (myocardial necrosis) = myocardial infarction (cell death from lack of blood flow) - Occurs when a coronary artery is totally obstructed (thrombus or embolus) - Atherosclerosis is the most common cause - Size and location of the infarct determine the damage - Classification - STEMI (ST-elevation myocardial infarction)  - Non-stemi (non-ST-elevation myocardial infarction - Classification determines the treatment and prognosis History of chest pain - Intense and unremitting for 30-60 minutes - Retrosternal and often radiating to the neck, shoulder, and jaws and down the left arm - Describe the pain as squeezing, aching, burning Epigastric: a feeling of indigestion of fullness and gas Others: nausea, vomiting, diaphoresis Often occurs early morning GOALS - To determine the presence or absence - To characterize the locus, nature, and extent - To detect recurrent ischemia or MI - To detect early or late complications - To estimate the prognosis Laboratory testing - 12 Lead EKG- an important tool in initial evaluation and triage - Cardiac biomarkers - troponin - test of choice - CK-MB - Complete blood count - Comprehensive metabolic panel - Lipid profile HEART FAILURE - Inability of the heart to pump enough blood to meet the body's needs (inadequate cardiac output) → inadequate perfusion of tissues - Usually a complication of another cardiopulmonary condition - Risk factors include ischemic heart disease and hypertension Pathogenesis - insufficient stroke volume (less pumping/ejection) - Less filling of the ventricles (heart) Anatomical - Left sided heart failure - Right sided heart failure - Both pumps fail- biventricular failure  - High cardiac output: heart failure due to acute non-cardiac origin Function - Systolic dysfunction - Heart failure with low ejection fraction (HFrEF) - Ejection fraction