Cardiovascular Physiology and Pathophysiology PDF

CARDIOVASCULAR PHYSIOLOGY and PATHOPHYSIOLOGY BY Dr LSK  CARDIOVASCULAR SYSTEM (CVS) The CVS consists of: The pump (heart or Vessels cardiac/tubes part),(blood &...

CARDIOVASCULAR PHYSIOLOGY and PATHOPHYSIOLOGY BY Dr LSK  CARDIOVASCULAR SYSTEM (CVS) The CVS consists of: The pump (heart or Vessels cardiac/tubes part),(blood & The blood vesselslymphatic vessels) consist of: a series of distributing and collecting tubes arteries, arterioles, venules and veins) the capillaries thin vessels that permit rapid exchange between the tissues and the vascular channels. The CVS = circulatory system  CVS DIVISIONS For descriptive purposes, CVS can be divided into two main parts: 1. The blood CVS the heart the blood vessels through which the blood flows. 2. The lymphatic system lymph nodes lymph vessels through which colourless lymph flows. BLOOD AND LYMPH VESSELS Function of CVS??? General Overview of CVS  INTRODUCTION The cardiovascular system is one of the first body systems to appear within the embryo. It is active by the beginning of the fourth week – when the placenta is unable to meet the requirements of the growing embryo. The development of the heart begins with the formation of the primitive heart tube following the folding of the embryo during the end of the third week The cardiovascular system is mesodermally derived Specifically, lateral splanchnic mesoderm… Gilbert fig 14.1 The cardiogenic field is established in the mesoderm just after gastrulation (~18-19 days) and develops into a fully functional, multi-chambered heart by the 8th week angiogenic cell clusters (angioblasts/hemangioblasts) (right endocardial tube) (right dorsal aorta) blood islands (developing blood vessels) pericardial cavity cardiogenic field Langman’s fig 12-1  FORMATION OF THE HEART TUBE The heart is the first functional organ to develop. It develops from splanchnic mesoderm (cardiogenic area), cranial to the developing mouth & nervous system and ventral to the developing pericardial sac. The heart primordium is first evident at 18 days (as an angioplastic cords which soon canalize to form the 2 heart tubes). As the head fold completed, the developing heart tubes lie in the ventral aspect of the embryo, dorsal to the developing pericardial sac. After lateral folding of the embryo The 2 heart tubes fuse together to form a single endocardial heart tube. It begins to beat at 22 to 23 days. Blood flow begins during the beginning of the fourth week and can be visualized by Ultrasound Doppler Cardiac Structures The heart valves Valvular heart disease (VHD): damage or defect in one of the four heart valves, aortic, mitral, tricuspid or pulmonary.  AV valves: Tricuspid and Bicuspid  Semilunar Valves: Aortic and Aortic  TYPES OF HEART VALVE DISEASE 1. Regurgitation incomplete valve closure backward flow of blood 2. Stenosis narrowing of the valve can be damaged, scarred, stiff 3. Atresia abnormal valve opening: Usually: congenital  DISORDERS OF HEART VALVES Mitral Valve Prolapse 16  CAUSES OF VALVULAR HEART DISEASE Rheumatic disease Endocarditis Congenital heart valve diseases Autoimmune diseases such as lupus is a disease that occurs when your body's immune system attacks your own tissues and organs Marfan syndrome: is a multi-systemic genetic disorder that affects the connective tissue)  RISK FACTORS FOR VHD Age Sex Family history Lifestyle Medical devices Other health conditions Radiation treatment  CLINICAL MANIFESTATIONS If VHD develops slowly person may be asymptomatic but if it develops acutely person may have: Exertional shortness of breath Angina Light-headedness or syncope Fatigue Palpitations Fever Edema Weight gain (loss in children) Heart failure  MANAGEMENT OF VHD Therapeutic goals for treating VHD: Symptom reduction Repairing or replacing valves Preventing blood clots Prevent irreversible LV changes which may result in further severe adverse cardiac events  MANAGEMENT OF VHD MEDICAL MANAGEMENT: Beta Blockers/Beta Adrenergic blocking agents Calcium channel blockers Digoxin Diuretics  MANAGEMENT OF VHD SURGICAL INTERVENTIONS: Aortic valve surgery Mitral valve repair surgery Annuloplasty Commissurotomy Tricuspid valve surgery Heart valve replacement surgery  Heart As a Pump Endocardi um Myocardium (Heart muscle) Epicardium Pericardi (Visceral Pericardial pericardium) Parietal cavity um Fibrous pericardium pericardium (Pericardial sac) Structure of the The pumping activity of heart wall Hypertrophic cardiomyopathy the heart (HCM)?  Fetal Circulation & Postnatal Changes  Fetal Cardiovascular system is designed: 1-To serve prenatal needs. 2-To permit modifications at birth, which establish the neonatal circulation.  Three structures are very important in the transitional circulation: 1- Ductus venosus. 2- Ductus arteriosus. 3- Foramen ovale. Two other important structure for fetal circulation 1. Umbilical vein 2. Umbilical artery  Blood reaches & leaves the fetus through the umbilical cord. The umbilical cord Contains :  two arteries and  one vein.  Highly oxygenated blood passes from the placenta through the umbilical vein. Ductus venosus Half of this blood reaches the IVC through the ductus venosus.  The other Half passes to liver sinusoids then to the IVC. Blood of the IVC reaches the right atrium, then left atrium through the Foramen Ovale. Then to the left ventricle to the ascending aorta, and the aortic arch to supply head & neck brain, cardiac muscle and upper limbs.  Small amount of highly Ductus arteriosus oxygenated blood in right atrium mixes with venous blood of the SVC passes to right ventricle. Then to the pulmonary artery then to Ductus Arteriosus (between the Pulmonary trunk & Proximal part of the descending aorta), to the fetal body. Then back to placenta via the umbilical arteries.  After Ligation of the umbilical cord Sudden fall of blood pressure in the IVC and the right Atrium. The valve of the ductus venosus constricts. After Aeration of the lungs at birth: 1- Marked increase in the pulmonary blood flow. 2- Dramatic fall in pulmonary vascular resistance. 3- Thinning in the wall of the pulmonary arteries. CHANGES AT BIRTH 34 35  Changes After Birth 1- Closure of foramen ovale: a. Physiological closure b. Anatomical closure. 2- Constriction of ductus arteriosus: By the end of the first 24 hours 20% of the lumen of the ductus is closed. By the end of 48 hours, 82% is closed. By 96 hours, 100% of the duct is closed Bradykinin: It is a substance released from fetal lungs during their initial inflation. This substance has a contractile effect on smooth muscles of the ductus arteriosus. The action of this substance appears to be dependant on the high Oxygen saturation of the aortic blood. MAJOR CARDIAC ANOALIES Risk Factors  Trisomy 21  Rubella virus during pregnancy 39  Atrial Septal Defects (ASD) Absence of septum primum and septum secundum, leads to common atrium. Absence of Septum Secundum-partial separation of atria  Patent foramen ovale In up to 20% of healthy adults, the foramen ovale will not completely close. We refer to this as a patent foramen ovale. Large, or slightly displaced “holes” in the septum are called atrial septal defects. While these may be asymptomatic, they can cause tachypnoea, poor weight gain, and recurrent chest infections in children and adults  VENTRICULAR SEPTAL DEFECT (VSD) Roger’s disease Absence of the membranous part of interventricular septum. Usually accompanied by other cardiac defects.  TETRALOGY OF FALLOT Blue Baby Fallot’s Tetralogy: 1-VSD. 2- Pulmonary stenosis. 3-Overriding of the aorta 4- Right ventricular hypertrophy. TETRALOGY OF FALLOT Blue Baby TETRALOGY OF FALLOT 45  (TGA) OR TRANSPOSITION OF GREAT TGA is due to abnormal ARTERIES rotation or malformation of the aorticopulmonary septum, so the right ventricle joins the aorta, while the left ventricle joins the pulmonary artery. It is one of the most common cause of cyanotic heart disease in the newborn. Blue Often associated with ASD Baby or VSD.  Persistent Truncus  It is due to Arteriosus failure of the development of the aorticopulmonary (spiral) septum.  It is usually accompanied with VSD.  Conduction System of the Heart Signal delay of ~ 0.09s oc The Electrical signals arise in the sinoatrial node (SA node). SA node is located in the superior posterolateral portion of RA below & slightly lateral to the opening of the superior vena cava. From the SA node, the impulses spread radially through RA Internodal along ordinary atrial myocardial pathways fibers. Anterio r Middle Posteri or Base Apex RBB- Right bundle branch LBB- Left bundle  Factors affecting heart conduction Sympathetic Norepinephrine increases IcaL through β1 receptors. Parasympathetic acetylcholine reduces the IcaL but improves Ik, leading to hyperpolarization. Increased temperature, caffeine & nicotine increase discharge frequency, while drugs such as Digitalis depress nodal tissue, particularly on the AV node. IE increase the contraction of heart muscles  Conduction disorder It is a problem with the electrical system that controls your heart’s rate and rhythm. In conduction disorders, the electrical signal either does not get produced properly, does not travel the way it should through the heart, or both. Types of conduction disorders  Sick sinus syndrome (SSS), also known as sinus node disease, affects the heart's natural pacemaker and causes slow heartbeats.  Atrioventricular (AV) block: This happens when no signals reach your ventricles.  Bundle branch blocks: These happen when the electrical signals travel more slowly in one side of the heart than in the other, causing your ventricles to contract at different times than TYPES Types of arrhythmias and dysrhythmias are identified by site of origin 1. SA NODE- originates from the Sinoatrial node  Sinus bradycardia- an impulse at a slower rate than normal rate (less than 60b/min)  sinus tachycardia- an impulse at a faster rate than the normal rate 2. Atrial arrhythmias- originate from the atria  Atrial tachycardia- is an unusually fast heartbeat that originates in the atria or chambers of the heart.  atrial flatter- caused by conduction defect in the atrium and causes a rapid atrial rate  atrial fibrillation- Is an irregular and often very rapid heart rhythm  Cont… 3.atrioventricular junction--- originates in the atrioventricular junction  junctional bradycardia(heart block)– heart beats slowly than usual  Junctional tachycardia ( wolf Parkinson’s white syndrome)— there is an extra electrical pathway between the atria and the ventricles Heart block – interruption of A-Ventricular conduction. Can generally be caused by 1. Ischemia of the A-V node or A-V bundle fibers 2. Compression of the A-V bundle by scar tissue or by calcified portions of the heart 3. Inflammation of the A-V node or A-V bundle 4. Extreme stimulation of the heart vagus nerves  Types of Heart Block A. 1st degree AV block- An abnormal prolongation of AV conduction time (long PR interval). i.e. conduction from atria to ventricles is delayed. B. 2nd degree AV block- Only a fraction of the atrial impulses are conducted to the ventricles. A ventricular beat may follow atrial beat (2:1 or 3:1). C. 3rd degree (complete) AV block- None of the atrial impulses reach the ventricles over a substantial number of atrial depolarizations. This can be due to septal myocardial infarction, damage to the bundle of His, AV nodal disease or strong vagal, (parasympathetic) stimulation. It is associated with syncope (Stokes-Adams attacks). Commonly requires artificial pacemaker. D. Bundle branch blocks – may be due to a degenerative process or due to coronary artery disease. They are LBB block, RBB block and fascicular block/hemiblock (block in anterior or posterior fascicule of LBB). 1st & 2nd AV blocks are most frequently caused by inflammatory processes (acute rheumatic fever), drugs (calcium channel antagonists), rapid atrial rates (supraventricular tachycardias) or weak vagal stimulation. Tetrodotoxin does not affect the action potentials in this region.  TERMS IN ECG P- Wave: represents the electrical depolarization of the atria. IE atrial contraction PR Interval: the time between atrial depolarization and ventricular depolarization. It represents the beginning of the P-wave and the beginning of the QRS complex PR segment: the portion of the ECG from the end of the P wave to the beginning of the QRS complex. Also part of atrial depolarisation QRS complex: Electrical depolarization of the ventricles when both ventricles contract T-wave: ventricle repolarization Absolute refractory period: The interval from the beginning of the QRS complex to the apex of the T wave QT interval: The time between the start of the Q wave and the end of the T wave. This is how long it takes for the heart to squeeze and refill with blood before it beats again.  Five steps Method of ECG 1. Identify and examine the P-wave: inverted and flat means dysrhythmia such as Junctional rhythm. 2. PRI: to measure: count no of small boxes multiply by 0.04 sec. ( Normal should be 0.20 sec. anything more than this indicates heart block 3. QRS complex: No of small boxes multiplied by 0.04 sec ( 0.06-0.12) Anything above this range is a dysrhythmia, such as A premature ventricular complex (PVC), which is a premature beat arising from an ectopic focus within the ventricles. AKA: ventricular ectopic 4. Rhythm ( either regular or irregular): measure the distance btw 2Rs. Using paper and pen or calliper. 5. Heart rate determination: divide 300 by the no of big boxes between 2Rs ABNORMAL ECGS  ARRHYTHMIAS Cont…. 4. Ventricles arrhythmias– rhythm originates in the ventricles  ventricular tachycardia – defined as 3 or more premature ventricular complexes in a row occurring at a rate exceeding 100bpm  Ventricular flutter- tachycardia affecting the ventricles with a rate over 250-350bpm  Ventricular fibrillation- rapid ,disorganized ventricular rhythm causes ineffective quivering of the ventricles CAUSES OF ARRHYTHMIAS Heart attack Blocked arteries in your heart High blood pressure Sleep apnea Smoking Drug abuse Drinking too much alcohol or caffeine Genetics Anxiety or stress SIGNS AND SYMPTOMS Palpitations Chest pains Shortness of breath Feeling of anxiety Dizziness hypotension Diaphoresis Fatigue MANAGEMENT OF ARRHYTHMIA Treatment of arrhythmia is directed at cause. The need for treatment varies : it is guided by symptoms and risks of the arrhythmia. Management can include avoiding triggering stimulants e.g. reduce or stop tobacco use, reduce excessive caffeine, exercising Antiarrhythmic drugs e.g. sodium channel blockers, potassium channel blockers. Ion supplements incase of problems with electrolytes levels. PROCEDURES AND DEVICES NEEDED IN MANAGEMENT OF ARRHYTHM Pacemakers Catheter ablation Cardioversion  COMPLICATIONS Some mild arrhythmias may not cause any health complication but more severe arrhythmias can if not treated. Cardiomyopathy Weakening of the heart muscles Heart failure Having an arrhythmia results in difficulty of the heart to effectively pump blood to the organs and tissues of the body. Stroke In some types of arrhythmia, it’s possible that blood can pool in the chambers of the heart, increasing the risk of blood clots, which can trigger a stroke if they travel to the brain.  COMPLICATIONS Pulmonary embolism A blockage in one of the arteries in your lungs due to blood clot Sudden cardiac arrest A sudden cardiac arrest can progress to death if it’s not promptly treated. Dementia Some arrhythmias are linked with dementia and other types of cognitive problems. Arrhythmias that get worse An existing arrhythmia can worsen over time or lead to another type of arrhythmia.  What is hypertension? A consistent elevation of the systolic blood pressure above 140mmhg and a diastolic blood pressure above 90mmhg Blood pressure is determined by cardiac output and systematic vascular resistance. These variables change to maintain BP reasonable to perfuse tissues.  Pathophysiology of hypertension The sympathetic nervous system and the renal renin angiotensin system provide overall control Cardiac output and peripheral vascular resistance are the primary regulating factors. Baroreceptors within the carotid sinus and the aortic arch, along with chemoreceptors in the medulla oblongata, sense changes in the blood pressure and cause the vaso-motor centre to respond to those changes through the sympathetic and parasympathetic nervous system. The renin-angiotensin system contributes to the control of blood pressure through the production of angiotensin II and the production of aldosterone, which leads to sodium and water retention, resulting in increased blood pressure. Types of Hypertension There are two types: Primary Hypertension also called Essential Develops gradual with no identifiable cause. Secondary High blood pressure that result from underlying conditions or a specific cause. e.g. Kidney disease, Hormonal disorders(hyperthyrodisim), medications  Risk Factors Age: middle to elderly. This is due to a decrease in blood vessel compliance Race: Blacks due to high intake of sodium diet Higher genetic susceptibility Physical inactivity which leads to cardiac workload Tobacco use: nicotine increases blood pressure also chemicals in tobacco cause vascular resistance Excessive alcohol consumption  Symptoms & Treatment Usually asymptomatic in early stages, but symptoms may occur such as Fatigue Malaise Morning headaches Treatment lifestyle changes :reduce salt intake, body weight and stress, increase cardiovascular fitness. Medications are individualized : one can be put on mild diuretics such as thiazide diuretics (antihypertensive action) ACE inhibitors are recommended as initial treatment. One or more medications can be used: Alpha blockers cause vasodilation, Calcium blockers reduce heart action and peripheral resistance Beta-blockers reduce heart action and sometimes renin release. Arterial Disease Disruption of the arterial blood flow can result from narrowing or complete obstruction of the wall of the blood vessel. It can be from a variety of causes, e.g. atherosclerotic plague, thrombus or embolus. Examples: Carotic artery disease, Peripheral artery disease & Aneurysm.  Peripheral Artery Disease (PAD) It is a slow and progressive circulation disorder caused by narrowing, blockage and spasms in a blood vessel. This loss of circulation can lead to gangrene or loss of a limb. Pathophysiology Formation of atherosclerotic plaque cause thickening of the arteries (normally femoral and iliac arteries) This leads to partial or complete obstruction of the vessel lumen, also this calcification of the atherosclerotic also weakness the arterial walls, leading to formation of thrombus. The disease occurs segmental and this affects blood flow, the body compensates through vasodilation to try and improve blood supply to the affected areas. As the diseases progresses, the symptoms also progress, and they may include: Pain (intermittent claudication – aching or grumping pain). Sensory impairment – tingling, burning and numbness Redness of the skin when they are lowered. Management of PAD Lifestyle modifications: stop smoking, exercise, diet changes(heart healthy diet) Pharmacological: antiplatelet agents (aspirin), statins (atorvastatin), anti-hypertensives (ace inhibitors), diabetes management. Surgical interventions: angioplasty /bypass/amputation  Venous Diseases Venous disorders result from malfunction/incompetent valves in the veins. This leads to obstruction of venous return to the heart which usual leads to a thrombus. Examples are Deep vein thrombosis (DVT) & varicose veins. Deep Vein Thrombosis Signs and Symptoms Pain or tenderness in the affected area Unilateral oedema Redness and warmth Complications Pulmonary Embolism (PE) –very fatal. The clot normally develops elsewhere but travels to the lung vessel causing blockage Management of Deep Venous Thrombosis Medications Lifestyle changes Anticoagulation therapy exercise Thrombolytic therapy – thrombolytic are Weight management administered to dissolve Avoid prolong immobility clot. Compression stockings Mechanical interventions Inferior vena cava filter use Catheter- directed Follow-up & monitoring thrombolysis Thrombectomy  Cardiac Failure/Heart failure (HF) HF is the reduced ability or inability of the heart to pump enough blood to meet the body’s needs. That is, reduced CO. It is usually caused by decreased contractility of the myocardium resulting from diminished coronary blood flow which leads to ischemia & infarction. However, it can also be caused by damaged heart valves, external pressure around the heart, vitamin B deficiency, primary cardiac muscle disease, etc. Divisions – Acute vs Chronic 1. Acute moderate cardiac failure  reduced cardiac output- can lead to cardiogenic shock Compensation – to restore normal CO without external aid Stimulation of Sympathetic and inhibition of parasympathetic activities  Chronic Heart Failure Begins after few minutes Compensation (1) Moderate fluid retention by the kidneys to increase VR & CO Large fluid retention as the heart weakens further can be detrimental (as it increases heart workload and causes oedema). (2) Varying degrees of recovery of the heart itself over a period of weeks to months through: the development of new collateral blood supply and hypertrophy of the undamaged portion of the heart musculature. As the heart recovers The water retention diminishes and the normal circulatory dynamics will be maintained despite the heart weakness so far the person remains at rest. Signs of failure might be seen during exercise.  Other Types of HF Compensated vs Decompensated HF Decompensated HF The HF continues to worsen because the heart becomes severely damaged and no amount of compensation restores a normal CO. Thus, a major cause of decompensated heart failure is failure of the heart to pump sufficient blood to make the kidneys excrete the necessary amounts of fluid every day. Continuous oedema (pulmonary and systemic) occurs, and the heart is overworked, leading to bubbling rales (a crackling sound) in the lungs, dyspnea (air hunger) and complete heart failure. Treatment of Decompensation Administration of A. diuretic drugs B. ACE inhibitors. C. Angiotensin II antagonists D. aldosterone receptor blockers. E. β –adrenergic receptor blocker Reducing venous tone with nitrates. Administration of a cardiotonic drug, such as digitalis Treatment of low-output failure (within the 1h) Not beneficial after 3h Digitalis is often administered Infusion of whole blood or plasma Infusion of BP–raising drug to sustain AP (to maintain coronary flow). Surgically removing the clot in the coronary artery Coronary bypass graft Catheterizing the blocked coronary artery Infusing either streptokinase or tissue-type plasminogen activator enzymes that cause dissolution of the clot.  Circulatory Shock Means generalized inadequate blood flow through the body tissues. It damages the tissue including the CVS. Also results in inadequate removal of wastes. Causes 1. Reduced CO (more often) due to : 1. Cardiac abnormalities, as many as 70 percent of people who experience cardiogenic shock do not survive. 2. Factors that decrease VR. 2 excessive metabolic rate than a normal CO 3 abnormal tissue perfusion patterns- most of the CO pass through blood vessels besides those that supply the local tissues. Stages of shock 1. A nonprogressive stage (compensated stage) – recovery without external therapy 2. A progressive stage- shock becomes steadily worse without therapy 3. An irreversible stage  Nonprogressive/Compensated Shock General compensatory mechanisms which maintain CO and AP are: All reflexes that maintain CO and AP (both the short-term and long-term). Readjustment of blood volume by absorption of fluid from the interstitial spaces & GIT oral ingestion and absorption of additional water and salt Recovery eventually takes place naturally, provided the shock does not become severe enough to enter the progressive stage. Pathophysiology of Progressive Shock  Types of shock 1. Hypovolemic shock – usually caused by hemorrhage decreases Venous Return & CO. Also caused by: A. Loss of plasma from the circulatory system, due to : 1. Intestinal obstruction and distension 2. Severe burns skin 3. General dehydration which results from: (a) excessive sweating, (b) severe diarrhoea or vomiting, (c) excess loss of fluid by the kidneys, (d) inadequate intake of fluid and salts (e) destruction of the adrenal cortices, with loss of aldosterone secretion. B. Trauma with or without haemorrhage. Compensation Sympathetic Reflex Compensations to raise Arterial Pressure Effect of hemorrhage on CO does not cause significant constriction of either the cerebral or the & AP cardiac vessels.  2. Neurogenic Shock Mainly due to loss of vasomotor tone which leads to increased vascular capacity (massive dilation of vessels especially veins) - venous pooling of blood. The reduced vascular capacity reduces the mean systemic filling pressure, which reduces VR and thus CO. Some neurogenic factors that can cause loss of vasomotor tone include the following: 1. Deep general anesthesia 2. Spinal anesthesia that blocks the sympathetic nervous 3. Brain damage – results from concussion or contusion or ischemia. 3. Obstructive shock –inadequate cardiac output as a result of obstruction of blood flow in the blood vessels (especially veins), in the lungs or in the heart.  4. Anaphylactic and histamine shock Anaphylaxis is an allergic condition in which the cardiac output and arterial pressure often decrease drastically. It results primarily from an antigen-antibody reaction during which the basophils in the blood and mast cells in the pericapillary tissues break down to release histamine or a histamine like substance. The histamine causes (1) an increase in vascular capacity (2) dilation of the arterioles, resulting in greatly reduced arterial pressure; (3) greatly increased capillary permeability, with rapid loss of fluid and protein into the tissue spaces. Histamine shock is caused by large intravenous histamine injection. 5. Cardiogenic shock – Results from heart failure  6. Septic shock – second to cardiogenic This term refers to a bacterial infection widely disseminated to many areas of the body, with the infection being borne through the blood from one tissue to another and causing extensive damage. Most cases of septic shock are caused by Gram-positive bacteria, followed by endotoxin producing Gram-negative bacteria. As a result of toxins from the bacteria, there is resultant loss of plasma into the infected tissues through deteriorating blood capillary walls reducing blood volume. Some of the typical causes of septic shock include the following: 1. Peritonitis caused by spread of infection from uterus, oviduct, GIT 3. Generalized bodily infection resulting from spread of a skin infection such as streptococcal or staphylococcal infection. 4. Generalized gangrenous infection resulting specifically from gas gangrene bacilli spreading from peripheral tissue to the liver and blood. 5. Infection spreading into the blood from the kidney or urinary tract, often caused by colon bacilli Special Features of Septic Shock. 1. High fever 2. generalized vasodilation 3. High CO in half of patients 4. Sludging of the blood, caused by red cell agglutination 5. Development of micro-blood clots in widespread areas of the body In early stages of septic shock, the patient usually does not have signs of circulatory collapse but only signs of the bacterial infection. General Treatment of Shock Transfusion of blood, plasma and/plasma substitute such as dextran solution. Use of sympathomimetic drugs in anaphylactic and neurogenic shock Head-Down Position- placing the patient with the head at least 12 inches lower than the feet. Oxygen therapy Administration of Glucocorticoids to increase the strength of the heart in the late stage of shock stabilize lysosomes in tissue cells aid in the metabolism of glucose by the severely damaged cells.  Circulatory Arrest- all blood flow stops Can occur as a result of cardiac arrest or ventricular fibrillation. In the case of complete cardiac arrest a normal cardiac rhythm can sometimes be restored by: immediately applying cardiopulmonary resuscitation procedures, while at the same time supplying the patient’s lungs with adequate quantities of ventilatory oxygen. In general, more than 5 to 8 minutes of total circulatory arrest can cause at least some degree of permanent brain damage in more than half of patients while if as long as 10 to 15 minutes, it almost always permanently destroys significant amounts of mental power. The permanent damage is mainly as a result of intravascular clotting.