Chapter 16: Alterations in Blood Pressure

Primary and Secondary Hypertension

• Primary (essential) hypertension has no identifiable cause and accounts for 90-95% of hypertension cases.

• Secondary hypertension is caused by an underlying condition, such as kidney disease, hormonal disorders, or certain medications.

Hypertensive Urgency vs. Emergency (Crisis)

• Hypertensive urgency is characterized by severely elevated blood pressure (systolic BP >180 mm Hg and/or diastolic BP >120 mm Hg) without signs of end-organ damage. Management includes oral antihypertensive medications and close monitoring.

• Hypertensive emergency (crisis) is characterized by severely elevated blood pressure with evidence of end-organ damage. This condition requires immediate intravenous antihypertensive treatment and hospitalization.

Symptoms of Hypotension

• Dizziness, lightheadedness, fainting, fatigue, blurred vision, nausea, and cold, clammy skin.

End Organ Damage of Hypertension

• Commonly affected organs include the heart (resulting in heart failure, coronary artery disease, or left ventricular hypertrophy), kidneys (leading to kidney failure), eyes (causing retinopathy), and brain (causing stroke or dementia).

End Organ Hypertension

• Heart: Hypertension increases the workload on the heart, leading to left ventricular hypertrophy (LVH), coronary artery disease, and heart failure.

• Kidneys: Hypertension can damage the blood vessels in the kidneys, impairing their ability to filter waste and regulate electrolytes. Over time, this can progress to chronic kidney disease or kidney failure.

• Eyes: Hypertensive retinopathy can occur when high blood pressure damages the blood vessels in the retina, potentially leading to vision impairment or blindness.

• Brain: Prolonged hypertension increases the risk of cerebrovascular events, such as stroke, and can also contribute to cognitive decline and dementia.

Modifiable Risk Factors in Hypertension Management

• Obesity, physical inactivity, high-sodium diet, smoking, and excessive alcohol consumption. Addressing these risk factors can significantly improve blood pressure control.

Blood Pressure Classification Ranges (ACH)

• Normal: systolic BP <120 mm Hg, diastolic BP 80 mm Hg

• Pre-hypertension: systolic BP 120-129 mm Hg, diastolic BP <80 mm Hg

• Stage 1 hypertension: systolic BP 130-139 mm Hg, diastolic BP 80-89 mm Hg

• Stage 2 hypertension: systolic BP ≥140 mm Hg, diastolic BP ≥90 mm Hg

Importance of Sodium in Hypertension

• Sodium plays a key role in fluid balance and blood pressure regulation. High sodium intake can lead to fluid retention, increased blood volume, and elevated blood pressure. Reducing sodium consumption can help lower blood pressure.

High sodium intake can contribute to hypertension through several mechanisms, as explained below:

1. Renin-Angiotensin-Aldosterone System (RAAS): Sodium levels influence the activity of the renin-angiotensin-aldosterone system (RAAS), a hormonal system that regulates blood pressure, fluid balance, and electrolyte homeostasis. When sodium levels are high, it suppresses the release of renin, a hormone secreted by the kidneys. However, if sodium intake is chronically high, it can lead to an imbalance in the RAAS, which may contribute to hypertension.

2. Fluid Retention: Increased sodium intake leads to an increase in extracellular fluid volume as the body tries to maintain the balance of sodium and water. The increased fluid volume puts additional strain on the blood vessels and the heart, leading to an increase in blood pressure.

3. Kidney Function: The kidneys play a critical role in regulating blood pressure by controlling the excretion and reabsorption of sodium and water. High sodium intake can impair kidney function, reducing its ability to excrete excess sodium and water effectively. This results in increased blood volume, which in turn elevates blood pressure.

4. Vascular Resistance: High sodium intake can also directly affect the blood vessels by increasing vascular resistance, which is the resistance offered by the blood vessels to blood flow. This can happen due to an increase in the production of reactive oxygen species and the subsequent reduction in the bioavailability of nitric oxide, a potent vasodilator. As a result, blood vessels become more constricted, causing blood pressure to rise.

5. Sympathetic Nervous System Activation: High sodium intake has been shown to stimulate the sympathetic nervous system, which can increase heart rate, vascular resistance, and renal sodium retention, all of which contribute to elevated blood pressure.

Action of ACE Inhibitors

• ACE inhibitors work by blocking the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This leads to vasodilation, decreased blood volume, and reduced blood pressure. Common side effects include a dry cough, dizziness, and hyperkalemia. Contraindications include pregnancy, bilateral renal artery stenosis, and angioedema.

Complications of Orthostatic Hypotension

• Falls, syncope, and injury. Management and prevention strategies include encouraging slow position changes, prescribing medications to raise blood pressure, suggesting compression stockings, and promoting adequate hydration.

Chapter 18: Alterations in Cardiac Function

Pulmonary Stenosis

• Failure of the valve to open completely results in extra pressure work for the heart — usually due to abnormal fusion of the valvular cusps and can lead to right ventricular hypertrophy

• Pulmonary stenosis is a congenital heart defect characterized by a narrowing of the pulmonary valve, which connects the right ventricle to the pulmonary artery.

• This narrowing obstructs blood flow from the right ventricle to the lungs, causing the right ventricle to work harder and potentially leading to right ventricular hypertrophy.

• Symptoms may include shortness of breath, fatigue, and chest pain. Treatment options include balloon valvuloplasty or surgical valve repair or replacement.

The correlation of LDL levels and coronary artery disease

• Low-density lipoprotein (LDL) cholesterol, often referred to as "bad" cholesterol, is a significant risk factor for coronary artery disease (CAD).

• Elevated LDL levels can lead to the formation of atherosclerotic plaques in the coronary arteries, which can narrow and stiffen the arteries, restricting blood flow to the heart muscle.

• Over time, this can cause angina, myocardial infarction, or heart failure. Management strategies include lifestyle modifications and medications to lower LDL cholesterol levels.

• LDL insudation occurs with oxidation by endothelial cells and macrophages.

Stable Angina vs. Unstable Angina

• Stable angina - chronic occlusion of a coronary vessel. Characterized by stenotic atherosclerotic coronary vessels

• Occurs when there is a predictable pattern of chest pain, elicited by similar stimuli each time, typically triggered by physical exertion or emotional stress, and relieved by rest or nitroglycerin. Chronic occlusion of a coronary vessel.

• Unstable angina is characterized by a sudden increase in the frequency, duration, or intensity of anginal episodes, or angina that occurs at rest. It is considered a medical emergency, as it may be a precursor to myocardial infarction. Acute occlusion results in unstable angina. May progress to acute ischemia.

Complications of Acute Coronary Syndrome

• Acute coronary syndrome (ACS) associated with acute changes in plaque morphology and thrombosis; abrupt and can be life-threatening leading to unstable angina and myocardial infarction.

• Acute coronary syndrome (ACS) refers to a spectrum of conditions resulting from decreased blood flow to the heart muscle, including unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).

• Complications of ACS may include heart failure, arrhythmias, cardiogenic shock, rupture of the heart muscle, and sudden cardiac death.

• Chest pain usually more severe and lasts longer than typical angina, Plaque rupture with acute thrombus development

• Unstable angina—occlusion is partial — MI—occlusion is complete

• ECG and biomarkers used for diagnosis

• not relieved by rest or nitroglycerin

Diagnostic tests and findings to detect Myocardial Infarction (MI) (heart attack)

• Electrocardiogram (ECG): Detects changes in the electrical activity of the heart, such as ST-segment elevation or depression and T-wave inversion.

• Cardiac biomarkers: Blood tests measuring the levels of troponin, creatine kinase-MB (CK-MB), and myoglobin, which are released into the bloodstream when heart muscle is damaged.

• Echocardiogram: Uses ultrasound to visualize the heart's structure and function, assessing wall motion abnormalities or ventricular dysfunction.

• Coronary angiography: Invasive procedure that involves injecting a contrast dye into the coronary arteries to identify the location and extent of blockages.

Rheumatic Heart Disease

• Diseases of the Endocardium

• Rheumatic heart disease is a condition resulting from damage to the heart valves caused by an autoimmune response to a group A β-hemolytic streptococci infection, such as strep throat or scarlet fever.

• The immune response mistakenly attacks the heart valves, leading to inflammation, scarring, and eventual dysfunction of the affected valves. Damage is due to immune attack on the individual’s own tissues. Antibodies against the streptococcal antigens damage connective tissue in joints, heart, skin. Occurs mainly in children.

• Symptoms may include chest pain, shortness of breath, distinctive truncal rash, involuntary movements (Sydenham chorea), and fatigue. Treatment options involve antibiotics to treat the infection, anti-inflammatory medications, and valve repair or replacement surgery if necessary.

Describe the different congenital heart defects (Example: Patent Ductus Arteriosus)

• Abnormality of the heart that is present from birth

• Acyanotic Congenital Defects: Disorders that result in left-to-right shunting of blood or obstruction to flow are generally acyanotic

• Patent ductus arteriosus (PDA): A persistent opening between the aorta and pulmonary artery that normally closes shortly after birth. Conditions that cause low blood oxygen tension may contribute to continued patency. No clinical significance in early life. Continued patency identified by harsh, grinding systolic murmur or thrill. This defect can lead to increased pulmonary blood flow, causing right sided heart failure and pulmonary hypertension if left untreated.

• Atrial septal defect (ASD): An abnormal formation at the opening (foramen ovale) between the right and left atria, allowing oxygen-rich blood from the left atrium to mix with oxygen-poor blood in the right atrium. This can cause increased blood flow to the lungs, leading to pulmonary hypertension and right heart failure, right ventricular hypertrophy, and reversal to a right-to-left shunt if left untreated.

• Ventricular septal defect (VSD): Most common congenital cardiac anomaly. A hole in the septum between the right and left ventricles, located in the membranous septum, near the bundle of His, causing oxygen-rich blood to mix with oxygen-poor blood. Increase in pulmonary blood flow can result in pulmonary hypertension, right ventricular hypertrophy, and reversal of the shunt

• Coarctation of the aorta: Narrowing or stricture of the aorta that impedes blood flow, Commonly located just before or after the ductus arteriosus, Upper extremities typically have an elevated blood pressure; lower extremities have weak pulses and low blood pressure, Usually accompanied by systolic murmurs and ventricular hypertrophy.

• Pulmonary Stenosis or Atresia:

  • Pulmonary atresia—blood must enter the lungs by traveling through a septal opening and a patent ductus arteriosus. Pulmonary stenosis—usually due to abnormal fusion of the valvular cusps and can lead to right ventricular hypertrophy

• Aortic Stenosis or Atresia:

  • Aortic atresias: not compatible with survival.

  • Aortic stenosis: involve the valvular cusps or the subvalvular fibrous ring and results in high left ventricular afterload with left ventricular hypertrophy Prominent systolic murmur

• Cyanotic Congenital Heart disease: Disorders that result in right-to-left shunting of blood result in cyanosis

• Tetralogy of Fallot: A combination of four heart defects, including pulmonary stenosis (which severity is related to degree of this), ventricular septal defect, aorta positioned above the ventricular septal opening, and right ventricular hypertrophy. This complex defect causes oxygen-poor blood to be pumped to the body, resulting in cyanosis, fatigue, and shortness of breath. Surgical intervention is necessary to correct the defects.

  1. Transposition of the great arteries: A condition where the aorta (arises from right ventricle) and the pulmonary artery (arises from left ventricle) are connected to the wrong ventricles, resulting in oxygen-poor blood being circulated to the body and oxygen-rich blood returning to the lungs. Incompatible with life. This condition causes cyanosis and requires surgical correction, such as the arterial switch operation.

  2. Truncus arteriosus: Failure of the pulmonary artery and aorta to separate; results in formation of one large vessel that receives blood from both the right and left ventricles. Results in systemic cyanosis.High pulmonary blood flow may cause pulmonary hypertension and right ventricular hypertrophy. Surgery required for survival.

  3. Tricuspid atresia: Usually associated with underdevelopment of the right ventricle and an atrial septal defect. A defect in which the tricuspid valve is absent or abnormally formed, preventing blood flow from the right atrium to the right ventricle. This results in oxygen-poor blood being mixed with oxygen-rich blood, leading to cyanosis. Treatment involves a series of surgical procedures to redirect blood flow and improve oxygenation.

Chapter 19: Heart Failure and Dysrhythmia

Symptoms of right and left-sided heart failure:

• Left-sided heart failure is characterized by the inability of the left ventricle to pump blood efficiently to the rest of the body. This can lead to increased pressure in the pulmonary circulation, resulting in pulmonary congestion and edema. Symptoms of left-sided heart failure include shortness of breath, orthopnea (difficulty breathing when lying down), paroxysmal nocturnal dyspnea, fatigue, and weakness.

• Right-sided heart failure occurs when the right ventricle fails to pump blood effectively to the lungs for oxygenation. This leads to increased pressure in the systemic venous circulation, causing peripheral edema, ascites, hepatomegaly, and jugular venous distension. Symptoms of right-sided heart failure include swelling of the ankles, legs, and abdomen, as well as weight gain and general fatigue.

Paroxysmal nocturnal dyspnea:

• Paroxysmal nocturnal dyspnea (PND) is a sudden and severe shortness of breath that occurs during sleep, typically in patients with left-sided heart failure. PND is caused by the accumulation of fluid in the lungs (pulmonary edema) due to the left ventricle's inability to pump blood effectively. This causes patients to wake up gasping for air, and they may need to sit up or stand to relieve the symptoms.

Reduced cardiac output in heart failure:

• Cardiac output is the amount of blood pumped by the heart per minute, and it's crucial for maintaining adequate blood flow and oxygenation to the body's tissues. In heart failure, the heart's pumping function is compromised, leading to a reduction in cardiac output.

• Several pathophysiological mechanisms contribute to reduced cardiac output in heart failure, including decreased contractility of the heart muscle, increased preload or afterload, and structural abnormalities in the heart.

• Reduced cardiac output can result in decreased blood flow and oxygen delivery to vital organs, leading to symptoms such as fatigue, weakness, and exercise intolerance. It can also cause a compensatory increase in heart rate, which may further exacerbate the heart's dysfunction.

Complications of dysrhythmias:

• Dysrhythmias, or abnormal heart rhythms, can disrupt the normal electrical conduction system of the heart, impairing its ability to pump blood effectively. Some complications associated with dysrhythmias include:

• Reduced cardiac output: Dysrhythmias can decrease the efficiency of the heart's pumping action, leading to reduced blood flow and oxygen delivery to vital organs.

• Heart failure: Persistent or severe dysrhythmias can strain the heart muscle and contribute to the development or worsening of heart failure.

• Blood clots and embolism: Dysrhythmias, such as atrial fibrillation, can cause blood to pool in the heart chambers, increasing the risk of clot formation and embolism, potentially leading to stroke or other serious complications.

• Cardiac arrest and sudden death: Life-threatening dysrhythmias, such as ventricular fibrillation or sustained ventricular tachycardia, can cause the heart to stop pumping blood effectively, leading to cardiac arrest and sudden death if not treated promptly.

Chapter 20: Shock

Signs and symptoms of anaphylactic shock:

• Anaphylactic shock is a severe and life-threatening allergic reaction that occurs when the immune system overreacts to an allergen. Common triggers include certain foods, medications, insect stings, or latex.

• Signs and symptoms of anaphylactic shock can develop rapidly and include difficulty breathing, swelling of the face, lips, or tongue, hives or rash, rapid or weak pulse, low blood pressure, dizziness or fainting, nausea, vomiting, or diarrhea, and a feeling of impending doom.

• The pathophysiology of anaphylactic shock involves the release of histamine and other inflammatory mediators from mast cells and basophils, leading to widespread vasodilation, increased vascular permeability, bronchoconstriction, and systemic hypotension.

Risk factors and pathogenesis of anaphylactic shock:

• Risk factors for anaphylactic shock include a history of allergies or previous anaphylaxis, asthma, and family history of anaphylaxis.

• The pathogenesis of anaphylactic shock involves an initial sensitization to an allergen, followed by a subsequent exposure that triggers a rapid and massive release of inflammatory mediators from mast cells and basophils. These mediators cause vasodilation, increased vascular permeability, and bronchoconstriction, leading to hypotension, respiratory distress, and potentially multiorgan dysfunction.

Define sepsis and septic shock:

• Sepsis is a life-threatening condition caused by the body's overwhelming response to an infection, which can lead to tissue damage, organ failure, and death.

• Septic shock is a severe form of sepsis characterized by profound circulatory, cellular, and metabolic abnormalities, including hypotension that is unresponsive to fluid resuscitation, and a high risk of mortality.

Types of obstructive shock:

• Obstructive shock occurs when a physical obstruction impedes blood flow, leading to reduced cardiac output and tissue hypoperfusion. Types of obstructive shock include:

• Cardiac tamponade: Accumulation of fluid in the pericardial sac compresses the heart, impairing its ability to fill and pump blood.

• Tension pneumothorax: Air trapped in the pleural space causes increased intrathoracic pressure, compressing the heart and great vessels, and reducing venous return.

• Pulmonary embolism: A blood clot or other embolus obstructs the pulmonary artery or its branches, reducing blood flow to the lungs and increasing right ventricular afterload.

Cardiogenic shock:

• Cardiogenic shock is a state of inadequate tissue perfusion due to the heart's inability to pump blood effectively, often resulting from severe damage to the heart muscle, such as a large myocardial infarction.

• The pathophysiology of cardiogenic shock involves a decrease in cardiac output, leading to reduced tissue perfusion and activation of compensatory mechanisms, such as increased heart rate, vasoconstriction, and fluid retention. These compensatory responses can further strain the heart and exacerbate the shock state.

• Treatment for cardiogenic shock may include medications to improve heart function, mechanical circulatory support devices, or revascularization procedures to restore blood flow to the damaged heart muscle.

Sample Quiz:

Question 1 Hypertension with a specific, identifiable cause is known as _______ hypertension. Answer: Secondary

Question 2 Hypotension associated with neurogenic and anaphylactic shock is due to _________ Answer: peripheral pooling of blood.

Question 3 Cardiac dysrhythmias are significant since they (select all that apply) Answer: as they have been ascribed to a direct toxic effect of cocaine and a secondary sensitization of ventricular tissue to catecholamines, along with slowed cardiac conduction secondary to local anesthetic effects.

Question 4 Cardiogenic shock is characterized by Answer: primary myocardial dysfunction leading to inadequate cardiac output.

Explanation: Decrease in cardiac output, which reduces the quantity of blood that can be pumped to different parts of the body. This can lead to an accumulation of fluid in the lungs, kidneys, and other organs. Cardiogenic shock can occur when too much blood flows out of a heart with less than normal pumping action (cardiac tamponade), when a severe life-threatening arrhythmia called ventricular fibrillation sends rapid chaotic contractions that prevent any significant flow from reaching the body (ventricular tachycardia or ventricular fibrillation), or when extreme dilation of a large left-sided heart chamber prevents any significant flow from reaching the body (acute mitral valve regurgitation).

Question 5 A patient has a history of falls, syncope, dizziness, and blurred vision. The patient’s symptomology is most likely related to _________

Answer: Orthostatic hypotension.

Explanation: The patient falls when they stand up, gets dizzy when they change positions and has blurred vision due to a drop in blood pressure. When standing up, blood rushes to the head and pools in areas not conducive to managing balance, such as joints or bone marrow. Blood pools because of gravity and a decrease in a sympathetic tone responsible for constricting veins and arteries. Orthostatic hypotension can be seen in patients with autonomic dysfunction which is seen later on down the line with Parkinson's disease or multiple system atrophy (MSA).

Question 6 The most reliable indicator that a person is experiencing an acute myocardial infarction (MI) is _________ Answer: if they experience acute chest pain that lasts more than 20 minutes.

Explanation: One of the most common symptoms associated with an MI is indigestion. These two symptoms, along with some other things, like nausea and difficulty breathing, are collectively referred to as the cardiac triad because they indicate a heart ailment of some sort. But what exactly is it? It's complicated but the short version is that an MI occurs when blood flow to part of your heart muscle dies because there's not enough oxygen or blood supply. This in turn can cause a change in the shape and function of your heart muscle, leading to your heartbeat becoming either irregular or too fast for its own good, among other things.

Question 7 Hypertrophy of the right ventricle is a compensatory response to __. Answer: Pulmonary Stenosis.

Explanation: Right ventricular hypertrophy is the direct result of pulmonary disorders that increase pulmonary vascular resistance and impose a high afterload on the right ventricle . Aortic stenosis does not lead to right ventricular hypertrophy. Aortic regurgitation is not associated with right ventricular hypertrophy. Hypertrophy of the right ventricle is not a compensatory response to tricuspid stenosis.

Question 8 Orthostatic hypotension is a risk factor for:

Question 9:   Angiotensin Converting Enzyme inhibitors (ACE inhibitors) blocks the.   Answer:  ACE blocks the body's production of angiotensin II.

Angiotensin II is a hormone that circulates in the blood and has many effects on the cardiovascular system; its main role is to constrict blood vessels.

Question 10:  A patient presenting with fever, hypotension, and lactic acidosis is most likely to be experiencing what type of shock?   Answer: Septic Shock Explanation: Septic shock is a life-threatening condition that happens when your blood pressure drops to a dangerously low level after an infection

Question 11: It can be explained to a patient that high blood pressure increases the risk of (Select all that apply)

Answer:

 Heart Attack- High blood pressure damages arteries that can become blocked and prevent blood flow to the heart muscle.

 Stroke — High blood pressure can cause blood vessels that supply blood and oxygen to the brain to become blocked or burst.

 Heart failure — The increased workload from high blood pressure can cause the heart to enlarge and fail to supply blood to the body.

 Kidney disease or failure — High blood pressure can damage the arteries around the kidneys and interfere with their ability to filter blood effectively.

 Vision loss — High blood pressure can strain or damage blood vessels in the eyes.

 Sexual dysfunction — High blood pressure can lead to erectile dysfunction in men and may contribute to lower libido in women.

 Angina — Over time, high blood pressure can lead to heart disease including microvascular disease. Angina, or chest pain, is a common symptom.

 Peripheral artery disease (PAD) — Atherosclerosis caused by high blood pressure can lead to narrowed arteries in the legs, arms, stomach and head, causing pain or fatigue.

Question 12:  Sepsis has been recently redefined as_________.

Answer: Requiring Organ Dysfunction or Multiple Organ Dysfunction Syndrome

Question 13 Cor Pulmonale refers to ______.

Answer:

Hypertrophy of the right ventricle as a result of pulmonary hypertension

Question 14 A patient has a heart murmur of mitral stenosis. The murmur would be heard during:

A heart murmur caused by mitral stenosis would be heard during diastole. Mitral stenosis is a narrowing of the mitral valve, which is located between the left atrium and the left ventricle. This narrowing obstructs blood flow from the left atrium to the left ventricle during diastole, causing the characteristic murmur.

Question 15 The majority of cases of anaphylactic shock occur when a sensitized individual comes in contact with ________.

Answer:

Question 16 Patent ductus arteriosus is accurately described as an/a ___________.

Answer: communication between the aorta and the pulmonary artery.

Explanation: A patent ductus arteriosus is a normal channel between the pulmonary artery and the aorta that remains open during intrauterine life. A patent ductus arteriosus is not an opening or a stricture in the atria. Patent ductus arteriosus is an acyanotic congenital defect.

Question 17 Hypotension, distended neck veins, and muffled heart sounds are classic manifestations of ___________.

Answer: Cardiac Tamponade ***Cardiac Tamponade is also known as Beck's Triad.

Question 18 Restrictions of which electrolytes is recommended in the management of high blood pressure? Answer: Sodium Explanation: Sodium can increase high blood pressure since it is naturally on food.

Question 19 A patient with a history of myocardial infarction continues to complain of intermittent chest brought on by exertion and relieved by rest. The likely cause of this pain is ________.

Answer: Stable angina

Explanation: Stable angina happens when there is a lack of oxygen in the heart muscle.

Question 20 While hospitalized, an elderly patient with a history of myocardial infarction was noted to have high levels of low-density lipoproteins (LDLs). What is the significance of this finding?

Answer: Increased LDL levels are associated with an increased risk of coronary artery disease

Explanation: According to Framingham Heart Study, LDL and HDL are the basis of the risk of having coronary artery disease.