Cardiovascular System
Review of the Cardiovascular System
Heart
Anatomy
Heart functions as a pump for circulating blood in both pulmonary and systemic circulations.
Heart is located in mediastinum between lungs (cardiac notch) and is enclosed in double-walled pericardium sac.
Outer fibrous pericardium anchors to the diaphragm.
An inner cavity filled with serous membrane which secretes fluid to reduce friction during heartbeats and allows the heart to operate smoothly.
Visceral pericardium, the inner layer of the pericardium, directly covers the heart's surface and is continuous with the heart's epicardium.
Middle layer of the heart is the myocardium, composed of specialized smooth cardiac muscles cells which contract rhythmically to pump blood into arteries.
Left ventricular wall is thicker in order to generate the necessary pressure to pump blood throughout the systemic circulation, supplying oxygen-rich blood to the entire body.
The right ventricular wall, while thinner than the left, plays a crucial role in pumping deoxygenated blood to the lungs (pulmonary circulation) to oxygenate them.
Inner layer of the heart is the endocardium, which lines the chambers of the heart and is composed of endothelial cells that provide a smooth surface for blood flow.
Atrioventricular valves: These include the tricuspid valve (between the right atrium and right ventricle) and the mitral valve (between the left atrium and left ventricle), which prevent backflow of blood during contraction.
Semilunar valves: These include the pulmonary valve (between the right ventricle and pulmonary artery) and the aortic valve (between the left ventricle and aorta), which prevent backflow of blood into the ventricles after contraction.
Septum: The septum is a muscular wall that separates the left and right sides of the heart, preventing the mixing of oxygen-rich and oxygen-poor blood.
Conduction System
No nerves are present inside the conduction system, as it relies on specialized cardiac muscle cells known as pacemaker cells to initiate and propagate electrical impulses.
Desmosomes → specialized structures that facilitate adhesion between cardiac muscle cells, ensuring synchronized contractions and maintaining structural integrity of the myocardium.
Conduction of impulses can be picked up by external electrodes that measure the electrical activity of the heart (electrocardiogram), allowing for the assessment of heart rhythm and function.
Atrial contraction (depolarization) in P wave.
Ventricular contraction (depolarization) in QRS complex.
T wave → Represents repolarization or recovery phase.
Actual Conduction:
All cardiac muscle cells can initiate impulses, but normally the conduction system begins at the SA (Sino Atrial) node / pacemaker.
SA Node → Lies in right atrium and depolarizes (spreading pulse to atriums) according to sinus rhythm, which is around 70 beats a minute without autonomic nervous system influence.
AV Node → Acts as a gatekeeper, receiving impulses from the SA node and delaying the signal for approximately 0.1 seconds to allow the atria to contract fully before the ventricle contracts.
AV Bundle (Bundle of His) → Connects the AV node to the ventricles, transmitting the electrical impulses down toward the
Left and right bundle branches (Purkinje fibers).
Control of the Heart
Cardiac Control Center is located in the medulla of the brain, where it controls heart rate and force of contraction.
Baroreceptors in walls of aorta and internal carotid arteries detect blood pressure changes and send signals to the cardiac control center via stimulation of sympathetic and parasympathetic pathways, allowing the body to maintain homeostasis.
Sympathetic stimulation increases heart rate and contraction (tachycardia) while parasympathetic stimulation decreases heart rate (bradycardia).
Sympathetic / Beta1-adrenergic receptors in the heart are important for drugs like beta blockers.
Factors which may increase heart rate include stress, environment, chemicals, physical activity, pregnancy, excitement, and the release of hormones such as epinephrine and thyroid.
Parasympathetic (rest and digest) decreases heart rate (bradycardia) through vagus nerve.
Coronary Circulation
Cardiac muscle requires constant supply of oxygen and nutrients to conduct impulses and contract efficiently, but has very little storage capacity for oxygen.
Two major arteries are present which branch off the aorta immediately above aortic valve:
Left Coronary Artery: Supplies blood to the left side of the heart, including the left atrium and left ventricle.
Right Coronary Artery: Supplies blood to the right side of the heart, including the right atrium and right ventricle, as well as parts of the conduction system.
Many small branches extend inward from the large arteries to supply the myocardium and endocardium. Blood supply is greatest during diastole / relaxation.
Anastomoses or direct connections exist between smaller branches of the coronary arteries, allowing for collateral circulation that can maintain blood flow to the heart muscle in case of blockage or narrowing in a primary vessel.
Cardiac Cycle
The alternating sequence of diastole (relaxation) and systole (cardiac contraction).
Diastole (Part 2) → Atrias fill and all valves are closed.
Diastole (Part 3) → Increased atrial pressure opens AV valves and ventricles fill.
Systole (Part 1) → Atria contract and empty; ventricles full.
Systole (Part 2) → Ventricles begin contraction, pressure closes AV valves and atria relax.
Systole (Part 3) → ventricles contract, increased pressure in ventricles causes aortic and pulmonary valves to open ejecting blood into aorta and pulmonary artery.
Diastole (Part 1) → Ventricles empty and relax; aortic and pulmonary valves close.
Teacher version
Diastole (Part 1) → complete relaxation; increased atrial pressure and ventricles fill.
Systole (Part 2) → Atria contract and empty; ventricles are full. P wave.
Systole (Part 3) → Atria relax and ventricles begin contract; all valves are closed. QRS Complex.
Systole (Part 4) → Ventricles contract, forcing blood out of the heart; the aortic and pulmonary semi-lunar valves open. T wave.
Diastole (Part 5) → Ventricles empty and relaxed, valves closed.
Diastole (Part 6) → Atria fill with blood from the veins; the tricuspid and mitral valves are open.
Mediate Auscultation (“lubb-dupp”) result from closure of valves.
“Lubb” (S1) → AV Valve closure after ventricular contraction indicates the start of systole, while "dupp" refers to the closure of the aortic and pulmonary valves at the end of systole.
“Dub” (S2) → Closure of semilunar valves after ventricular systole, signaling the end of the heartbeat.
Murmurs: Abnormal sounds produced by turbulent blood flow in the heart, which can indicate underlying heart conditions such as valve abnormalities or congenital defects.
Pulse deficit → difference in rate between the apical pulse (heart rate measured at the apex of the heart) and the radial pulse (rate measured at the wrist), which can indicate poor perfusion or decreased cardiac output.
Cardiac output → The volume of blood the a ventricle pumps per minute, influenced by heart rate and stroke volume, playing a crucial role in overall cardiovascular health.
CO = SV x HR
Stroke Volume (SV) → the amount of blood ejected by the left ventricle during each contraction, which is an essential factor in determining cardiac output and overall heart efficiency.
Preload → Amount blood delivered to heart by venous return.
Afterload → Force required to eject blood from ventricles and is determined by peripheral resistance to opening of semilunar valves.
Contractility → How strong the force of the ventricles.
Heart Rate → How many times blood contracts a minute.
Blood Pressure
BP - no change = Increased cardiac output multiplied by decreased peripheral resistance.
BP - elevated = Neutral change in cardiac output multiplied by increased peripheral resistance.
IF: Increased heart rate (increased cardiac output) X systemic vasoconstriction (increased peripheral resistance) then increased BP.
IF: Decreased stroke volume (Cardiac Output) X decreased systemic vasodilation (peripheral resistance) then decreased BP.
Blood pressure is elevated by increased SNS in two ways:
SNS and epinephrine act on Beta-adrenergic receptors in heart to increase both the rate and force of contraction.
SNS, epinephrine, and norepinephrine increase vasoconstriction by stimulating the alpha1 receptors in the arterioles of skin and viscera; reduces systemic blood flow, which subsequently contributes to an elevation in blood pressure.
Hormones which influence Blood Pressure.
Antidiuretic hormone (ADH) increases water reabsorption through kidney and increases vasoconstriction, leading to an increase in blood volume and, consequently, an elevation in blood pressure.
Aldosterone increases blood volume by increasing reabsorption of sodium ions and water.
Renin-angiotensin-aldosterone system in kidneys regulates blood pressure by controlling blood volume and systemic vascular resistance, initiating a cascade that ultimately leads to increased blood pressure.
Diastolic Pressure → sustained pressure when ventricles relax.
Sustained pressured when ventricles relax.
Blood pressure (BP) altered by cardiac output, blood volume, and peripjeral resistance to blood flow.
BP = HR x SV x TPR
Systolic Pressure → sustained pressure when ventricles contract.
SNS BRANCH OF ANS
Increased output → vasoconstriction and increased BP.
Decreased output → vasodilation and decreased BP.
BP proportional to blood volume.
Heart Disorders
Heart failure: A condition where the heart is unable to pump sufficiently to maintain blood flow to meet the body's needs.
Myocardial infarction: Commonly known as a heart attack, occurs when blood flow to a part of the heart is blocked, resulting in damage to the heart muscle.
Arrhythmias: Irregular heartbeats that can disrupt normal blood flow, leading to various complications.
Diagnostic Tests for Cardiovascular Function
ECG → useful in initial diagnosis of arrhythmias, myocardial infarction, infection and pericarditis.
Stethoscope / auscultation of heart → Useful in detection of murmurs or abnormal shunts of blood.
Echocardiography → Used to record heart valve movements, blood flow and cardiac output.
Exercise stress tests → Useful for accessing general cardiovascular function and checking for exercise-induced abnormalities.
Cardiac imaging → Used to show shape and size of heart; Nuclear imaging and tomographic studies (CT scan)
Cardiac catherization → A procedure used to measure pressure and assess valve and heart functionality.
Determination of central venous pressure and pulmonary capillary wedge pressure.
Doppler studies → A non-invasive method used to assess blood flow and detect abnormalities in the heart and blood vessels.
Arterial blood gas determination → A test that evaluates the levels of oxygen and carbon dioxide in the blood, providing insight into the respiratory and metabolic status of the patient.
Drug Therapy
Vasodilators such as nitroglycerin or extended-release isosorbide reduce peripheral resistance systemically, reducing blood pressure while improving stroke volume.
Beta Blockers → Block beta1-adrenergic receptors in the heart, leading to a decrease in heart rate and contractility, thereby lowering myocardial oxygen demand and blood pressure.
Metoprolol and atenolol are common examples of beta blockers used in the management of hypertension and heart failure, providing protective effects on the cardiovascular system.
Treatment of hypertension and dysrhythmias; reduction of angina attacks.
Calcium channel blocker → Inhibit the influx of calcium ions into cardiac and smooth muscle cells, resulting in decreased contractility and vasodilation, which lowers blood pressure and relieves angina.
Skeletal muscle has far more calcium, thus not responding similarly to calcium channel blockers as cardiac muscle, which relies on calcium influx for contraction.
Prophylactic against angina.
Digoxin → A cardiac glycoside that increases the force of myocardial contraction and decreases heart rate by inhibiting the sodium-potassium ATPase pump, leading to increased intracellular calcium levels.
Used for heart failure and as an antiarrhythmic drug for atrial dysrhythmias.
Adrenergic-blocking drugs → Drugs which may act on SNS centrally (brain) by blocking peripheral (arteriolar) alpha1-adrenergic receptors or direct vasodilators.
ACE inhibitors → Block conversion of angiotensin I to angiotensin II, which reduces peripheral resistance and aldosterone secretion, ultimately leading to decreased blood pressure and fluid retention.
Treatment for hypertension and CHF.
Diuretics → Removes excess sodium and water by blocking of reabsorption of sodium or water. Treatment of high BP and congestive heart failure.
Anticoagulant / Blood-thinners → Reduced chance of blood clot formation.
Can be helpful with arrythmias.
Cholesterol-lowering drugs → Help prevent clotting from occurring by managing lipid levels in the bloodstream and reducing the risk of atherosclerosis.
Coronary Artery Disease
Arteriosclerosis → General term for all types of arterial changes.
Degenerative changes in small arteries and arterioles.
Loss of elasticity and lumen gradually narrows, allowing for obstruction or increased peripheral resistance.
Increased blood pressure and presence of atheroma in large arteries.
Atherosclerosis → Build-up of plaque consisting of fats, cholesterol, calcium and other substances on the artery walls.
Related to diet, exercise and stress.
LDL → Bad; HDL → Good.
Usually it begins with some inflammation or damage then a cascade begins.
Non-modifiable factors
Age and Gender; Males and postmenopausal woman increased risk.
Genetic and familial factors → Hypercholesteremia.
Modifiable factors
Obesity and sedentary lifestyle.
Smoking and oral contraceptives.
Synergistic effect: Smoking vasoconstricts and oral conceptive make blood viscous.
Diabetes mellitus and poorly controlled hypertension.
No chest pain until 75% blockage.
Grid flow
Atherosclerosis in Heart → Angina pectoris (ischemic heart disease).
Total occlusion → Myocardial infarction (MI)
Atherosclerosis in Brain (carotid or central arteries partial occlusion) → Transient Ischemic Attack (TIA) or Stroke.
Atherosclerosis in Peripheral Arteries → Peripheral Artery Disease (PAD) and Claudication.
Treatment:
Weight loss; increase exercise.
Dietary modification → Incorporating heart-healthy foods such as fruits, vegetables, whole grains, and lean proteins is essential for managing symptoms and improving overall cardiovascular health.
Medications → Statins, antiplatelet agents, and medications to improve blood flow can help manage PAD and reduce the risk of cardiovascular events.
Lifestyle changes → Quitting smoking and reducing alcohol intake are crucial steps towards enhancing heart health.
Control hypertension, lowering ldl and increasing hdl.
Surgical intervention → Bypass grafting.
Peripheral Vascular Disease
Disease in arteries outside of the heart.
Increased incidence with diabetes.
Most common sites → Abdominal aorta, carotid arteries and femoral/iliac arteries.
Treatments
Control of blood glucose levels.
Reduce BMI and cholesterol.
Cessation of smoking, exercise.
Platelet inhibition and peripheral vasodilators.
Angina Pectoris
Deficit of oxygen to meet myocardial needs.
Chest pain may occur in different patterns.
Classic or exertional angina
Variant angina
Vasospasm occurs at rest.
Unstable angina
Prolonged pain at rest
May precede myocardial infarction.
Recurrent, intermittent chest pain that may occur with exertion or emotional stress.
Attacks vary in severity and duration but become more frequent and longer.
Relieved by rest and administration of coronary vasodilators.
Example: nitroglycerin.
Potent vasodilator.
Decreases demand for oxygen.
Pallor, diaphoresis (excessive sweating), nausea and chest pain.
Emergency treatments!
Rest and stop activity. Patient seated in upright position.
Nitroglycerin — sublingual.
Check pulse and respiration.
Administer oxygen, if necessary.
Patient known to have angina → Second dose of NTG.
Third dose of NTG (20 minutes) → suspected MI.
Patient without history of angina → Emergency medical aid.
Myocardial Infarction
Death of myocardial tissue due to ischemia.
Coronary artery = totally obstructed.
Atherosclerosis is most common cause.
Thrombus from atheroma may obstruct artery.
Vasospasm is caused in a small percentage.
Size and location of infarct determine damage.
Signs differ between men and woman.
Men → Nausea/vomiting, jaw, neck or back pain, squeezing chest pressure or pain and shortness.
Woman → Chest discomfort, shortness of breath, fatigue, lightheadedness, and pain in the arms, back, neck, or jaw.
Left anterior descending artery → Widow maker.
Diagnostic testing
Changes in ECG → Lift off baseline.
Serum enzyme and isoenzyme levels.
Myosin and cardiac troponin are elevated due to cell death.
Some of these are changed during angina attacks as well.
Complications
Sudden death → arrhythmias and fibrillation.
Which kind? We messed with conduction system enough heart stops.
Cardiogenic shock → decreased cardiac output leading to inadequate tissue perfusion and potential multi-organ failure.
Congestive heart failure → a condition in which the heart is unable to pump sufficient blood to meet the body's needs, often resulting in fluid buildup in the lungs and other tissues.
Rupture of necrotic heart tissue / cardiac tamponade → wall becomes weakened enough and rupture.. leading to blood leaking into pericardial activity.
Thromboembolism - CVA with left ventricular MI.
Treatment
Reduce cardiac demand + oxygen therapy.
Analgesics and anticoagulants.
Thrombolytic agents may be used.
Tissue plasminogen activator.
Medication to treat:
Dysrhythmias and deep vein thrombosis, helping to dissolve blood clots and restore normal blood flow.
Cardiac Dysrhythmias: Irregular heartbeats that can affect the heart's ability to pump blood effectively, potentially leading to serious complications.
Can cause clotting or bleeding disorders, which may complicate treatment and require careful monitoring of the patient's condition.
Treatments include determine cause and prescribing specifically for that.
Other treatments like antiarrhythmic drugs can be used.
Beta-adrengenic blockers.
Calcium-channel blockers.
Sinus Node Abnormalities
SA node → Pace maker of the heart; rate can be altered.
Bradycardia → Regular but slow heart rate (<60).
Tachycardia → Regular rapid heart rate (>100)
Dependent on lifestyle.. those who run will naturally have a lower resting heart rate due to improved cardiovascular fitness, while individuals with a sedentary lifestyle may experience higher rates of bradycardia or tachycardia.
Sick sinus syndrome → Marked by alternating bradycardia and tachycardia. Typically requires mechanical pacemaker.
Atrial Conducton Abnormalities.
Atrial flutter → Atrial heart rate of 160 to 350 beats/min.
AV node delays conduction resulting in ventrcular rate slower. Indicicative of stroke.
Premature atrial contractions or beats (PACs, PABs)
Extra contraction from ectopic foci can lead to irregular heart rhythms, which may cause symptoms like palpitations or decreased cardiac output.
Atrial fibrillation → rate over 350 beats/min.
Pooling of blood present.
Atrioventricular Node Abnormalities
Heart blocks → Conduction delayed or stopped at AV node or bundle.
First-degree block → Delay.
Second-degree block → Partial pass-through;
Third-degree block → Nothing passing through.
Purkenjie fibers have natural rhythm has 30 beats a minute but not sufficient.. need pacemaker.
Bundle branch block → Interference with conduction in one of the bundle branches.
Ventricular tachycardia → likely to reduce cardiac output as reduced s
Ventricular fibrillation → Control removed from conduction system.
Muscle fibers conduct independently and rapidly.
Cardiac stand-still occurs if not treated as soon as possible.
Pre-mature ventricular fibrillation → Irregular heartbeats that can lead to insufficient blood flow and potential collapse, emphasizing the need for immediate medical intervention.
treatments include:
Cause needs to be determined and treated.
Anti-dysrhythmic drugs are effective in many cases.
SA nodal problems or total heart block require pacemaker.
Congestive Heart Failure
When heart cannot maintain pumping capability.
Less blood to organs in general.
Decreased cell function and fatigue.
Backup and congestion develop as coronary demands for oxygen and glucose are not met.
Output from ventricle < inflow of blood.
Congestion in venous circulation draining into affected side of the heart.
BACKUP EFFECTS.
Right-sided congestive effect heart failure → Systemic buildup.
Left-sided congestive heart failure → Pulmonary congestion, leading to symptoms such as shortness of breath and fluid accumulation in the lungs.
Forward effects → Decreased blood supply to tissues; hypoxia & fatigue, and dyspnea or shortness and breath.
Compensation mechanisms → Tachycardia.
Cutaneous and visceral vasoconstriction.
Daytime oliguria → hold onto fluids to increase blood volume, which can help improve perfusion to vital organs.
Backup effects of left-sided failure (LUNGS)
Related to pulmonary congestion.
Dyspnea and orthopnea → Develop as fluid accumulates in lungs.
Cough → associated with congestion due to dyspnea.
Paroxysmal nocturnal dyspnea
Indicates presence of acute pulmonary edema.
Usually develops during sleep.
This condition is characterized by sudden shortness of breath that may awaken the individual, prompting them to sit up to alleviate discomfort.
Signs of and Symptoms - Right (SYSTEMIC)
Dependent edema in feet, legs and buttocks.
Increased pressure.
Ascites → fluid accumulation in the abdominal cavity, leading to swelling and discomfort.
Acute right-side failure → flushed failure, distended neck veins, headache and visual disturbances.
Rheumatic Fever and Rheumatic Heart Disease
Rheumatic Fever → Acute systemic inflammatory condition.
May result from an abnormal immune reaction.
Can occur a few weeks after an untreated infection , particularly streptococcal throat infections, leading to complications such as heart valve damage.