Hemostasis: Blood Clotting and Bleeding Control

Chapter 14: Hemostasis

• Hemostasis is the process of stopping bleeding through blood coagulation.
• Hemostasis can occur via blood clot, vessel spasm, or physical means like compression/bandage.
• A blood clot is a meshwork of fibrin threads, plasma, and blood cells.
• Coagulation inhibitors are coagulation factors that restrict clotting.
• Plasmin dissolves fibrin and is formed when plasminogen is activated into plasmin (fibrinolysin).
• Thrombocytopenia means having a deficiency in platelets.
• Petechiae are small spots, indicating defective platelets, or a capillary defect.
• Von Willebrand disease is an autosomal dominant bleeding disorder caused by inadequate protein.
• Hematoma: Large hemorrhage that results from a deficiency of plasma coagulation factors.
• Intravascular means inside blood vessels and disseminated means widespread.

Factors Concerned with Hemostasis

• Key factors include small blood vessel integrity, which is the body's first defense.
• Also important are having enough platelets.
• Normal levels of coagulation factors and inhibitors and calcium are also required.

Important Platelet Functions

• Platelets plug defects in vessel walls.
• Platelets liberate vasoconstrictors and compounds, causing platelet aggregation.
• Platelets initiate coagulation by releasing necessary substances.

Blood Coagulation Process

• Phase 1: Prothrombin activator is generated through intrinsic (blood-derived) and extrinsic (tissue injury) systems.
• Both pathways activate simultaneously and interact to initiate the clotting process.
• Both pathways generate thromboplastin to form prothrombin activator.
• Phase 2: Prothrombin converts to thrombin.
• Phase 3: Fibrinogen converts into fibrin by thrombin.
• A blood clot forms at the end of Phase 3.

Coagulation Inhibitor Example

• Antithrombin is an example of a coagulation inhibitor.

Four Categories of Coagulation Disturbances

• Abnormalities include small blood vessel issues, abnormal bleeding, and abnormal vessel formation.
• Disturbances may also arise from platelet formation abnormalities.
• Deficiencies can occur in plasma coagulation factors.
• Thromboplastic material can liberate into circulation.

Causes of Thrombocytopenia

• Injury or disease of the bone marrow can damage megakaryocytes, the precursors of platelets.
• Bone marrow infiltration by leukemic/cancer cells crowds out megakaryocytes.
• Antiplatelet antibodies can destroy platelets in peripheral blood, resulting in an autoimmune disease.
• Abnormal platelet function despite normal platelet count can cause thrombocytopenia.

Phase 1 Disturbance: Hemophilia

• Hemophilia is an X-linked hereditary disease primarily affecting males, characterized by hemorrhage episodes in joints and internal organs after minor injuries.
• Hemophilia A is classic hemophilia, involving Factor VIII (antihemophilic factor).
• Hemophilia B, or Christmas disease, involves Factor IX (Christmas factor).

Phase 2 Disturbance

• Phase 2 disturbance arises from a deficiency of prothrombin or factors required for prothrombin to convert into thrombin.
• Factors necessary for Phase 2 are produced in the liver.
• Vitamin K is crucial for their synthesis.
• Vitamin K is synthesized by intestinal bacteria or obtained from food.
• Bile is needed for Vitamin K absorption.

Prothrombin Deficiency Indicators

• Anticoagulant drugs inhibit active clotting factors.
• Inadequate vitamin K synthesis occurs due to intestinal bacteria death from antibiotic use.
• Bile duct blockage inhibits vitamin K absorption.
• Impaired liver synthesis leads to inadequate coagulation factors.

Thromboplastic Activity

• Events with thromboplastic activity, liberating into circulation, result in intravascular coagulation.
• These events include diseases linked to shock, tissue necrosis, and overwhelming bacterial infections

Disseminated Intravascular Syndrome

• Disseminated Intravascular Syndrome is a rare clotting disorder leading to abnormal bleeding, preventing deadly clot formation.

Chapter 12: Diseases of Blood Circulation

• Virchow's triad refers to the three categories of factors contributing to thromboses.
• A thrombus is an intravascular clot.
• Thrombi usually form in the deep veins of the legs, known as deep venous thrombosis (DVT).
• An embolus is a detached clot blocking smaller blood canals, leading to necrosis.
• An infarct is tissue necrosis caused by blocked blood flow.
• Edema is a fluid accumulation in tissues, commonly presented as swelling.
• Shock is when the circulatory system fails to deliver enough blood to body parts and causes organ failure.
• Shock is always life-threatening.

Virchow's Triad Factors

• Slowing or stasis of blood flow.
• Blood vessel wall damage.
• Increased blood coagulability.

Predisposing Factors for Venous Thrombosis

• Prolonged bed rest or cramped positions.
• Impaired leg muscle "milking action" hinders venous return.
• Other factors include varicose veins and increased blood coagulability.
• Possible outcomes are pulmonary embolism and leg swelling from venous return blockage.
• In pulmonary embolism, a clot detaches and lodges inside the pulmonary artery.

Clinical Manifestation Dependence

• Clinical manifestations depend on the embolus size and location within the pulmonary artery.

Lung Damage from Pulmonary Emboli

• Large pulmonary emboli block blood flow, causing severe dyspnea, cyanosis, shock, and sudden death.
• Small pulmonary emboli block pulmonary arteries, leading to wedge-shaped pulmonary infarcts.
• If infarcts develop, symptoms are dyspnea, pleuritic chest pain, cough, and hemoptysis.

Diagnosis and Treatment of Pulmonary Emboli

• Chest X-rays detect infarct but not the embolus itself.
• Radioisotope lung scans detect abnormal pulmonary blood flow caused by embolism.
• Pulmonary angiograms are the gold standard for detecting blocked pulmonary arteries.
• Computed tomography (CT) detects pulmonary embolism by showing obstructed contrast medium flow.
• Treatment includes general supportive care, anticoagulation, thrombolytic drugs, and surgery for large embolisms.

Main Cause of Arterial Thrombus

• Arterial thrombus formation is mainly caused by arteriosclerosis, through injury to the vessel wall.

Types & Effects of Arterial Thrombus

• Coronary artery thrombus leads to myocardial infarction.
• Major leg artery thrombus leads to gangrene.
• Cerebral artery thrombus leads to stroke.

What is Gangrene

• Gangrene is tissue death caused by blood flow loss due to illness, injury, or infection.
• It typically affects fingers, toes, and limbs but can also affect other body art.

Causes & Results of Intracardiac Thrombi

• Clots form within atrial appendages, heart valve surfaces, or the ventricular wall.
• Portions may dislodge into systemic circulation and lead to infarction in the spleen, kidneys, or brain.

Factors Increasing Thrombosis Risk

• Raised levels of coagulation factors follow surgery or injury due to thromboplastin release.
• Estrogen in contraceptive pills or pregnancy stimulates clotting factor synthesis.
• Hereditary gene mutations can cause abnormal factor V Leiden.

Genetic Factors Increasing Thrombosis Risk

• Factor V Leiden mutation results in factor V resistance and increased coagulability.
• Mutation of genes regulating prothrombin synthesis also increases the risk.
• A raised prothrombin level leads to greater venous thrombosis.

Thrombosis in Cancer Patients

• Higher levels of coagulation factors and platelets in cancer patients lead to risk.
• It predisposes patients to both arterial and venous thrombosis.
• The hypercoagulability comes from tumor deposits releasing thromboplastic materials.
• Tumors release thromboplastic material continuously, causing production of coagulation factors to exceed destruction.

Causes of Edema

• Edema disturbances arise from the extracellular fluid circulation between capillaries and interstitial fluid.

Factors Regulating Fluid Flow

• Capillary hydrostatic pressure pushes fluid into the extracellular space.
• Capillary permeability dictates fluid flow through the endothelium.
• Osmotic pressure attracts water exerted by blood proteins, drawing fluid from the interstitial back into capillaries.
• Open lymphatic channels collect fluid and return it to circulation.

Types of Edema

• Pitting edema leaves an indentation upon fingertip compression.
• Pleural effusion (hydrothorax) involves fluid accumulation in the pleural cavity.
• Ascites is fluid accumulation in the peritoneal cavity.

Four Causes of Edema

• Increased capillary permeability can cause swelling of tissues.
• EX: Acute inflammation or systemic disease
• Low plasma proteins causes excess protein loss or inadequate synthesis.
• EX: Kidney disease, malnutrition, or liver failure
• Increased hydrostatic pressure may arise from heart failure or localized venous obstruction.
• Lymphatic obstruction blocks fluid return from the interstitial space.
• EX:

Categories, Causes and Shock

• Shock results from low blood pressure.
• Its result is inadequate organ/tissue perfusion.

Hypovolemic Shock

• Hypovolemic shock is caused by low blood volume, which leads from hemorrhage, dehydration, severe burns, diarrhea and diuretic use.

Cardiogenic Shock

• Cardiogenic shock is inadequate cardiac output when the heart cannot effectively pump blood.
• It is caused by myocardial infarction (reducing pumping function) and pericardial effusion (prevents heart filling).

Septic Shock

• Septic shock is excessive vasodilation from release of microbial toxins and inflammatory mediators.

Anaphylactic Shock

• Anaphylactic shock is excessive vasodilation from release of inflammatory mediators caused by an allergic reaction.

Shock Signs & Symptoms

• Skin is cool, clammy, and pale.
• Weakness, dizziness, thirst and nausea are common.
• Breathing may be shallow and rapid, with a weak, rapid pulse.
• Blood pressure is low, and lips/fingernails can be cyanotic.
• Patients may be confused or suddenly unconscious
• Drugs like vasoconstrictors are used to help symptoms.
• Prognosis relies on early recognition and treatment.
• Treatments include fluids/blood and treatment of the underlying cause.

Chapter 11 Diseases of the Heart and Circulation

• Diastole is when the heart muscle relaxes.
• Systole is when the heart muscle contracts.
• Ischemia occurs when a body part gets insufficient blood.
• Dr. Bernard Lown invented the defibrillator and was a 1985 Nobel laureate.
• Cardiomyopathies causes mechanical and/or electrical dysfunction often causing ventricular hypertrophy/dilation and can stem from genetics, etc.

Heart Function

• The heart's primary function is to pump blood through the lungs and to the rest of the body.

Heart Layers

• Epicardium: outer connective tissue layer with coronary arteries.
• Myocardium: middle, muscular layer, workhorse of the heart.
• Endocardium: innermost, smooth layer that lines chambers and heart valves.
• Pericardium surrounds the heart in a double-walled sac reducing friction.

Right vs Left Circulations

• Right side: Pulmonary circulation
• Left side: Systemic circulation

Heart Valves

• Atrioventricular valves: tricuspid (RA to RV) and bicuspid/mitral (LA to LV).
• Semilunar valves: pulmonary (RV to pulmonary trunk) and aortic (LV to aorta).

Blood Flow Through the Heart

• Blood flows from the superior/inferior vena cava to the right atrium (RA).
• Then it goes through the tricuspid valve to the right ventricle (RV).
• From the RV, it passes through the pulmonary valve to the lungs.
• Next, it enters the left atrium (LA) and goes through the bicuspid/mitral valve to the left ventricle (LV).
• Finally, it goes through the aortic valve to the aorta.

Coronary Circulation

• Coronary circulation provides the heart its own blood supply.
• The right coronary artery (RCA) supplies the posterior wall and interventricular septum.
• The left coronary artery (LCA) branches.
• LCA supplies to the anterior wall and anterior interventricular septum . : LCA supplies to the lateral wall

Cardiac Conduction System

• Cardiac conduction consists of events associated with one complete heartbeat.
• Atrial systole atrial diastole ventricular systole ventricular diastole.
• Key components are SA node, AV node, bundle of HIS, and Purkinje fibers.

Phases of the Cardiac Cycle

• Diastole: Chambers relax, blood flows through open AV valves; SL valves are closed.
• Atrial Systole: Additional blood flows into ventricles.
• Ventricular Systole: Ventricles contract, AV valves close, SL valves open when pressure builds.
• Diastole: Chambers relax, SL valves close, AV valves open, and blood flows into chambers.

Types of Blood Vessels

• Large elastic arteries carry blood throughout the body.
• Arterioles regulate flow from arteries to capillaries.
• Capillaries deliver nutrients and remove waste with their endothelium.
• Veins return blood to the heart under low pressure.

Systolic vs. Diastolic Blood Pressure

• Blood flow in the arteries results from ventricular contractions.
• Systolic pressure is the highest when ventricles contract.
• Diastolic pressure is lowest when ventricles relax.

Electrocardiogram (ECG/EKG)

• Electrocardiograms measure the heart's electrical activity and identify disturbances in rate, conduction, rhythm, injury, and extent of muscle damage.
• The deflections of the ECG are labeled P, Q, R, S, and T.

Arrhythmias: Signs, Symptoms & Etiology

• Arrhythmias are any deviation from the normal sinus rhythm (heartbeat).
• Symptoms: palpitations, tachycardia, bradycardia, syncope, fatigue, skipped heartbeats.
• Etiology: interference within the conduction system of the heart, ischemia and drugs.

Normal Sinus Rhythm

• An electrocardiogram (ECG) reads within normal limits with a heart rate between 60-100 bpm.
• Sinus bradycardia causes a regular rhythm with a heart rate of <60 bpm.
• Sinus tachycardia causes a heart rate of >100 bpm.

Atrial Fibrillation

• Atrial fibrillation is seen in older persons, and patients with CVD, COPD, hyperthyroidism and causes rapid atrial contractions and atrial "quivering".
• An electrocardiogram shows small, irregular, disorganized P waves.
• Ventricles beat irregularly at 140-160 bpm during atrial fibrillation, leading to shortened filling time.
• The goal of treatment of arrythmia is to decrease heart rate and restore normal rhythm.
• A watchman device may be used for treatment.

PVCs and Cardiac Arrest

• Extrasystole characterized by a beat early in time, missing p wave.
• Is considered normal and is caused by stress, diet.
• Ventricular contraction characterized by 3 or more PVCs- can be life threatening.
• Rapid hearbeat is called cardiac arrest.

Medical Interventions

• Stoppage of drugs with the adverse affect drug induced arrhythmias.
• Electrical countershock- cardioversion- delivers electrical pulses in order to convert heartbeat.

Valvular Malfunction

• 2 types of valvular malfunction Stenosis: hardening of cusp and insufficiency (incompetence, regurgitation): valve not close.
• Rheumatic fever: antigen-antibody react injures connectivity in tissue, can cause inflammation/clinical outcomes and prevented with the right treatment.

Causes of Rheumatic heart Disease

• The rheumatic heart disease has valves become red then swollen- leads to stress on heart failure.
• It it prevented beta strep infection from occurring (leads to valve damage).

Types of non Rheumatic aortic

• Non-rheumatic: occurs if the heart has 2 valves instead of 3: this can lead to further complications such as heart stress failure.
• Mitral valve prolaspe : abnormal chord length that causes regurgitation.

Infective endocarditis

• Vegetations builds up in heart: bacterial is most relevant.
• Causes leaflet erosion and infection in blood.

Interventions for Sub endocarditis

• Those at high risk should receive sub acute for protection.
• Acute endocarditis is where the affecter is highly pathogenic- such as a drug users.

Hypertension

• High vascular and excessive amounts of smooth muscle from constrictive arterioles.
• Asymptomatic if occurs from genetic disease: risk include sedentary diseases.

Diagnosing elevated high pressure

• elevated BP> changes needed, with high BP risk comes 1-= year heart disease.
• Primary elevated pressure cause be a result of a BP control mechanism.
• The main BP control mechanisms are kidney, hormone control and thyroid.

Main points of hypotension

• Increased heart rate puts higher strain, leads to heart failure.
• Atherosclerosis increased, which then weakens area to the degree of potential harm.
• Goal through medication is dilation to ensure blood can move freely.
• Myocarditis: occurs from direct muscle inflammation, viral trigger and can lead to failure.

Types of cardiomyopathies:

• Muscle disease to the point of heart failure and hypertension on a number of issues.
• Hypertrophic cardiomyopathy: increases size can obstruct flow and cause block- usually asymptomatic.

Types of cardiac diseases;

• Ventricular failure- blood failure with systematic complications- causes lung blockage.
• The 4 main causes of congenital heart disease are: block age of flow.
• Causes a mixing and failure to close/complete- resulting in need for surgery with a heart replacement.
• There are 2 types of aneurysm: one side is not formed properly- need for drugs (smoking/stress).
• Thrombosis occurs in all vascular- can cause a dissecting damage leading to stroke.

Types of vessels disease: cause and how can we maintain.

• Vein have low pressure that can result in venous damages which can be treated through the intervention.
• Atherosclerosis is build pressure on walls arteries: this can lead to ruptures.
• Stable plaques do not rupture as often and can result in a high amounts of strokes.

Case Notes

• Angina is the first stage of cardiovascular disease.
• The goal of an interventions is for decrease the prelaod/afterload which overall reduces workload of heart.
• CHF or congestive heart failure has to do with stress on organ/organ failures.
• Pleural effusion: is caused from adima/liver problems.
• Anuria's is the increase is blood output with lack blood in blood.
• CHF occurs when heat isn't working right- one has high output during this instance, this can be reduced with good habits.