Cardiovascular System: Hypertension and Consequences

Introduction

• Kirsty McCray introduces herself as the tutor for pathophysiology and pharmacology for nursing.
• The tutorial focuses on hypertension and its consequences.
• Consequences include angina, ischemia leading to myocardial infarction (heart attack), and ultimately cardiac failure.
• Cardiac cells (cardiomyocytes) and vascular cells are non-regenerative, meaning damage is permanent.
• Early intervention is crucial to prevent myocardial infarction and heart failure due to limited treatment options at later stages.

Function of Cardiovascular System

• The cardiovascular system's primary function is to pump blood containing oxygen and nutrients to cells throughout the body.
• Blood from the systemic circulation enters the heart via the superior and inferior vena cava, flowing into the right atrium.
• From the right atrium, blood moves to the right ventricle and then into the pulmonary circulation for oxygenation in the lungs, where gas exchange occurs.
• In the lungs, carbon dioxide is removed, and oxygen binds to hemoglobin in red blood cells for transport to cells and tissues.
• Oxygenated blood returns to the left atrium, then to the left ventricle, and is pumped through the aorta into systemic circulation.
• The cardiovascular system relies on multiple body systems working together to regulate homeostasis.
• The primary function: deliver oxygen and nutrients; without these, cells undergo necrosis and die.

Blood Vessel Layers

• Understanding blood vessel layers is important for understanding atherosclerosis, hypertension, and myocardial infarction.
• Tunica Externa: Outermost layer containing fibroblasts and connective tissue.
• Tunica Media: Contains vascular smooth muscle cells, enabling contraction and relaxation of the blood vessel.
• Tunica Intima: Thin layer of endothelial cells that control hormone passage to vascular smooth muscle cells.
• Hormones from the peripheral nervous system (parasympathetic and sympathetic) regulate blood vessel contraction and relaxation.
• Sympathetic nervous system releases adrenaline, causing blood vessel contraction.
• Parasympathetic nervous system releases acetylcholine, leading to nitric oxide production, causing blood vessel relaxation.
  Blood flows from arteries to arterioles to capillaries (where oxygen and nutrient exchange occurs) to venules to veins, and back to the heart.
• Vena cava is the largest vein returning blood to the heart.

Blood Pressure

• Blood pressure is defined by systemic blood pressure, flowing from highest to lowest pressure.
• Highest pressure is in the aorta.
• Nurses measure blood pressure in arteries, divided into systolic and diastolic pressure.
• Pressure decreases from arteries to arterioles to capillaries; minimal pressure in venules and veins.
• Veins have valves to prevent backflow due to gravity and low pressure.
• Blood flows from highest to lowest pressure; gradient ensures blood flow.
• Measurements consist of systolic (e.g., 120) and diastolic (e.g., 80) blood pressure.
• Systole: Pressure during heart contraction (peak pressure by left ventricle).
• Diastole: Pressure during heart relaxation; diastolic pressure is most important as it reflects the heart's relaxed state.
• Normal blood pressure for a resting healthy adult is around 120/80, fluctuating with activity level, gender, stress and diet.

Factors Influencing Blood Pressure

• Baroreceptors: Respond to muscle stretching (e.g., during exercise).
• Chemoreceptors: Respond to changes in blood constituents (carbon dioxide levels, pH, oxygen levels).
• Nervous, renal, and respiratory systems collaboratively control blood pressure, focusing on cardiovascular, respiratory, and urinary systems.
• Kidneys detect blood pressure and initiate changes. Lungs, working with the central nervous system (CNS) via carotid bodies detect oxygen saturation.
• Low oxygen triggers the brain to signal the kidneys to release erythropoietin, increasing red blood cell production and oxygen transport.
• Kidneys release renin in response to low blood pressure; renin converts angiotensinogen (from the liver) to angiotensin I.
• Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE) mainly in the lungs, which is the major pressure hormone.
• Short-term blood pressure control involves baroreceptors and the sympathetic nervous system releasing adrenaline.
• Osmo-receptors in kidneys release antidiuretic hormone (ADH) and aldosterone to control blood constituents.
• ADH inhibits urination, retaining water to increase blood pressure.
• Aldosterone increases sodium reabsorption, leading to water reabsorption and increased blood pressure.
• The renin-angiotensin-aldosterone system (RAAS) is crucial; angiotensin II is beneficial short-term but detrimental long-term.
• Angiotensin II causes pathological changes in blood vessels and the heart, contributing to cardiovascular diseases.
• Obesity, hypertension, kidney failure/damage, and diabetes impact angiotensin levels and function.

Hypertension

• Hypertension is defined as a constant elevation in arterial blood pressure; hypotension is low blood pressure (not always bad).
• Elevated blood pressure damages blood vessels, leading to inflammation and atherosclerosis (non-reversible).
• Atherosclerosis leads to myocardial infarction, angina, and heart failure.
• Blood Pressure Classifications (mm Hg):
  • Normal: <120/80
  • Normal High: 120-129/80-84
  • Mild: <160/<100
  • Moderate: <180/<110
  • Severe: >180/>110
  • Isolated Systolic Hypertension: >140/<90
• Usually doctors recommend dietary and lifestyle changes for patients with normal high blood pressure.
• Pharmacological treatments usually commence in grades 1-3
• Measurements should not be based on one-off readings due to white coat syndrome (elevated blood pressure due to nervousness in clinical settings).

Types and Treatment of Hypertension

• Types of hypertension:
  • Primary (essential/idiopathic): No identifiable underlying cause; linked to genetics and lifestyle.
  • Secondary: Caused by an underlying condition (e.g., kidney disease).
  • Pregnancy-induced: Due to preeclampsia.
• Treatment strategies target systems affecting hypertension to prevent vascular damage and atherosclerosis.
• Metabolic Disturbances:
  • Often seen with metabolic syndrome (hypertension, obesity, diabetes).
  • Leads to insulin resistance and endothelial dysfunction.
  • Treated with exercise and dietary modifications (reduced salt, fat, and sugar intake).
• Neuro-hormonal Control:
  • Diuretics are used to reduce sodium and water retention.
• Overactive Renin-Angiotensin-Aldosterone System:
  • Angiotensin receptor blockers (ARBs) or ACE inhibitors are prescribed.
• Overactive Central Nervous System:
  • Calcium channel blockers or beta-blockers are used.

Hypertension Risk Factors

• Non-Modifiable Risk Factors:
  • Family history: Genetic predisposition.
  • Advancing age: Increased likelihood with age.
  • Hereditary and race
  • Gender: Males before 55, females after menopause.
• Modifiable Risk Factors:
  • Physical activity: Sedentary lifestyle increases risk.
  • Diet: High-fat, high-calorie diets increase risk.
  • Weight: Obesity increases risk.
  • Smoking: Increases risk.
  • Alcohol intake: Excessive consumption increases risk.
  • Fat and salt intake: Deviation from recommended intake increases risk.
• Health care providers recommend modifiable lifestyle changes.

Hypertensive Medications

• Hypertensive medications target the central nervous system (CNS), aldosterone, or RAAS.
• Common medication categories (ABCD):
  • A:
    • ACE inhibitors (e.g., captopril, ending in "-pril") target angiotensin-converting enzyme.
    • ARBs (e.g., candesartan, ending in "-sartan") are angiotensin II receptor blockers.
    • Alpha-agonists (e.g., clonidine) target alpha-adrenergic receptors.
  • B: Beta-blockers (e.g., atenolol, metoprolol, ending in "-olol") are beta-adrenergic receptor antagonists. Some are selective, targeting beta-1 receptors in the heart (atenolol, metoprolol), while others are non-selective (propranolol), affecting both beta-1 and beta-2 receptors in the heart and lungs, respectively.
    • Non-selective beta-blockers can limit asthma treatment options.
  • C: Calcium channel blockers (e.g., amlodipine, ending in "-ipine") inhibit blood vessel and heart contraction.
  • D: Diuretics (thiazide or loop diuretics like furosemide) act on the kidneys to reduce water and sodium retention.
• Many patients require multiple antihypertensive medications or combination pills (poly pills).
• Medications reduce blood pressure but do not address underlying causes (pro-inflammatory, pro-oxidative stress state).
• Doctors need to incentivise patients to undertake modifiable changes, complemented with pharmacological treatments.

Mechanism of Action

• Alpha-2 agonists decrease sympathetic impulses from the CNS, causing vasodilation.
• Alpha-1 blockers target sympathetic activation in arterial alpha-1 adrenergic receptors.
• Vasodilators (e.g., GTN) bypass endothelial cells to directly cause vasodilation in vascular smooth muscle cells.
• Calcium channel blockers inhibit calcium influx, reducing contraction.
• ARBs block angiotensin II receptors.
• ACE inhibitors prevent the conversion of angiotensin I to angiotensin II.
• Diuretics increase output and decrease fluid volume in the kidneys.
• Beta-blockers decrease heart rate and myocardial contractility.

Angina

• Angina is often caused by hypertension leading to atherosclerosis, classified as stable, unstable, or variant angina.
• Angina is cardiovascular pain due to reduced blood flow from vessel blockage.
  • Stable Angina: Most common, caused by atherosclerosis; pain occurs on exertion and is relieved by rest.
  • Unstable Angina: Caused by atherosclerosis with thrombosis (clot); compromised blood flow at rest; pain occurs without exertion and is not relieved by rest.
  • Variant Angina: Caused by vasospasm, where blood vessels spasm reducing the opening within the blood vessel, and may or may not involve atherosclerosis; pain can occur anytime, even during sleep, with no recognizable trigger.
• Treatments include nitrates (GTN), beta-blockers, calcium channel blockers, and potassium channel openers (agonists), causing vasodilation.

Progression of Cardiovascular Disease

• Atherosclerosis leads to obstruction, arterial spasms (sudden, reversible), or plaque splits with thrombosis (occlusion).
• All these lead to ischemia (reduced blood flow) and hypoxia (reduced oxygen in tissue).
• Hypoxia causes angina (pain) and potential thrombosis (blood clot).
• Unstable angina is caused by atherosclerosis and blood clots, leading to permanent thrombosis which leads to necrosis (tissue death).
  • Myocardial infarction (MI) occurs from necrosis, often due to thrombus dislodgement in the heart. If the thrombus dislodges and goes into the brain it causes stroke. If it goes dislodges into the lungs it can cause pulmonary embolism.

Consequences of Myocardial Infarction (MI)

• MI leads to impaired contractility, which in turn leads to thrombi which leads to stroke (brain).
  • Impaired contractility causes hypotension that leads to cardiogenic shock.
• Tissue necrosis (death of cardiac cells).
  *Papillary muscle infarction can cause congestive heart failure.
  *Electrical instability (arrhythmia, irregular heartbeat).
• Pericardial inflammation (pericarditis: inflammation of the pericardium).

Heart Failure

• Heart failure is usually what happens from chronic MIs. The tissue in the heart becomes damaged (necrosis from MIs) and it cannot function (contract) properly.
• It's a condition that develops over time, often starting with systemic inflammation, damaging blood vessels and leading to the atherosclerosis then progression of MIs.

Heart Failure Pathophysiology

• Chronic systemic infection and damage of the cardiovascular system leads into:
  • Systolic heart failure: Left ventricular ejection fraction (LVEF) < 40%; inability for the heart to contract properly,
  • Diastolic heart failure: LVEF > 50%; heart cannot relax properly.
  • Heart failure causes decrease cardiac output because the heart can not contract or relax
• Left-sided heart failure: Inadequate pumping of blood to the body, causing backflow in the pulmonary vein,
• Right-sided heart failure: Inadequate pumping to the lungs, causing backflow in peripheral veins and the liver.

Heart Failure Classification

• Class is categorized through 1-4 based on severity, with class 4 being the most serious.
• Class 4 includes patients with heart disease that cannot carry out physical activities without extreme discomfort.
• It's good to familiarize yourself with common medical abbreviations but it's also important to know there could be other abbreviations used depending on the hospital.

Compensatory Mechanisms and Terminology

• Declined oxygen, nutrients, and cardiac output because your heart does not contract and/or relax as a solid unit.
• Body increases the compensation system by activating or telling the CNS system and RAS, which causes more damage to the heart (pathological changes)..
• Preload and Afterload
• Preload: Volume of blood in the ventricles at the end of diastole (end-diastolic pressure); imagine blowing up a balloon.
  • increases when values are foulty
• Afterload: Resistance the ventricle must overcome to circulate blood; pressure required to pump blood into the aorta. Afterload stretches as heart is filling (valves filling)
  *Increases in hypertension because the blood vessels constrict making it harder for the heart to pump the blood out.

Compensatory Heart changes

• Activation of CND and RAS to increase blood pressure because of our heart issues.
• Blood does not perfuse as a solid unit (like it should).
• Compensatory hypertrophy of the myocardium is a part of pre- and afterload.

Neurological Aspects

• Because are heart is not function, therefore it is not getting enough oxygen since there is to much mass/heart fiber in the left ventricle.
• Tissue hypoxia (reduced) or anoxia (no oxygen) can cause infarction.
• This can lead to many of the previously mentioned heart complications.

Final Remarks

• Doctors do NOT diagnose patients on the spot. They have to send you home with tools to self-diagnose by measuring blood pressure to then come into the office with a week's work of blood pressure data. Then they will provide a REAL diagnosis.
• Arrhythmia's can be hard to catch in one take. Many have triggers to cause them, therefore can happen out of the blue. To catch them, they can take 24 hour ECG's. Medications are used to treat the different types of arrhythmia's by using sodium channel blocker, calcium channel blocker and/or a potassium channel blocker.
• Health-care takers provide the best care to their patients when they advise life style changes in addition to the medications they are prescribing.

Summary on Drug Effectiveness

• A summary was discussed. The drugs that people are commonly prescribed DO NOT have personalize data for everyone. People are typically are prescribed from the start with a beta blocker and then prescribed additional drugs depending on severity.