TREATMENT APPROACHES

The long, flat line between impulses indicates an abnormally slow heartbeat.

In some cases, arrhythmias may not require treatment. Other arrhythmias can be controlled by treating the underlying cause. Arrhythmias that cause symptoms may require one or more of the following treatments to reduce the number or duration of arrhythmic events.

Medications. Common medications for suppressing arrhythmias include:

• Beta-blockers;
• Calcium channel blockers;
• Digitalis; and
• Antiarrhythmic agents.

Digitalis should not be used for certain arrhythmias, such as WPW syndrome. People with atrial fibrillation are typically prescribed an anticoagulant to minimize their risk of clotting and stroke.

Cardioversion. This procedure restores a normal heartbeat by transmitting a brief electric shock through the chest to the heart. Usually an outpatient procedure that is performed in a hospital while the patient is under heavy sedation or anesthesia, it is commonly used to treat:

• Atrial fibrillation;
• Atrial flutter; and
• Ventricular arrhythmias.

Radiofrequency Catheter ablation. A catheter with an electrode tip is positioned on the affected area. The catheter delivers energy to destroy tissue that is interfering with the normal transmission of electrical impulses through the heart. It is most commonly used for:

• SVT – Supra Ventricular Tachycardia (Pulse over 100);
• Atrial fibrillation-particularly newly diagnosed;
• Atrial flutter; and
• Certain types of ventricular arrhythmias.

Catheter ablation for SVT utilizing radiofrequency ablation (electrocautery injury) was developed in the 1980’s and has since revolutionized the treatment of SVT. With catheter ablation, a procedure is performed entirely through intravenous catheters inserted into the veins in the leg and sometime the shoulder. It is a minimally invasive procedure. That is, no open heart surgery is needed. Generally, procedures can be performed on an outpatient basis. Overall cure rates with catheter ablation is >90% and can be as high as 96-98% depending on the specific type of SVT.

During a catheter ablation procedure, catheters (long wire electrodes) are advanced through the veins in the leg up to the heart.

Various measurements of the electrical system are performed. If a person is in normal rhythm at the time of the procedure, an attempt is made then to reproduce the SVT by pacing the heart through the catheters. Occasionally an intravenous medicine called isoproterenol is required to “rev up” the heart in order to reproduce the SVT. Once the SVT is reproduced, the specific type of SVT can be diagnosed using the catheters in the heart.

Once the SVT is diagnosed, to cure the SVT, an ablation catheter is advanced to the heart. An ablation catheter is capable of delivering small radiofrequency lesions (electrocautery burns) on the order of 4-5 mm in diameter. These radiofrequency lesions have no long-term adverse consequences. Depending on the type of SVT, these radiofrequency lesions are delivered in various locations of the heart.

Occasionally, more complex diagnostic and ablation techniques are required for catheter ablation of SVT. This may be the case particularly in patients with other heart problems or a history of heart surgery. In such situations, sophisticated 3-dimensional mapping techniques using a balloon catheter may be used to identify the location necessary to successful ablate the SVT

Pacemaker. A small electronic device that is surgically implanted under the skin near the collarbone. A pacemaker regulates a slow or erratic heartbeat by sending rhythmic electrical charges to the right atrium and right ventricle. Pacemakers are frequently used to treat Sick Sinus Syndrome.

Maze procedure. A physician makes multiple incisions through the atrium. The resulting scar tissue conducts impulses through the heart’s electrical system in a way that allows normal conduction but does not sustain atrial fibrillation. Since it is a form of cardiac surgery, it is reserved for those patients who have undergone a failed catheter ablation or as an add-on for those having a surgical procedure for another condition.

Cardiac arrhythmia, also known as cardiac dysrhythmia or irregular heartbeat, is a group of conditions in which the heartbeat is irregular, too fast, or too slow.

Susheel K. Kodali, MD is the co-director of the Heart Valve Center at NewYork-Presbyterian/ Columbia University Medical Center.

Ablation is used to treat abnormal heart rhythms, or arrhythmias. The type of arrhythmia and the presence of other heart disease will determine whether ablation can be performed surgically or non-surgically.

Ablation therapy using radio frequency waves on the heart is used to cure a variety of cardiac arrhythmiae such as supraventricular tachycardia, Wolff–Parkinson–White syndrome (WPW), ventricular tachycardia, and more recently as management of atrial fibrillation (especially when its newly diagnosed when medical management can’t change it back to normal sinus rhythm, which is the normal cardiac rhythm seen on a telemetry monitor or of an EKG taken on a patient).

An arrhythmia is a change in the heart’s normal rate or rhythm, normally between 60 and 100 beats per minute. Arrhythmias are classified by their location in the heart and by their speed or rhythm. An atrial arrhythmia is an abnormality that occurs in one of the two upper chambers of the heart, the left or right atrium. Arrhythmias are associated with aging and typically happen more frequently during middle age. At least 10 to 15 percent of people older than 70 years experience arrhythmias.  We have what we call our human pacemaker of the heart that naturally sends conduction for the heart to pump, which is called the sinus node.  This is in the upper left corner of the right chamber of the heart.  That is where the name sinus rhythm derives from (the sinus node) which is the best rhythm a human can be in as long as the pulse rate stays above 60 and stays under 100. Now if that sinus node for some reason breaks down and no longer works; so than the pace site starts somewhere in the right atrium below the sinus node (the heart is compensating for whatever is the reason the sinus node is not working).  So now the rhythms are called atrial rhythms because of where the new natural pacemaker site is in the heart.  This is where ablation comes into play if the type of atrial rhythm they have is detrimental to the patient; including if that patient is a candidate for this procedure.  Between our heart chambers on the top (called atriums) and below (called the ventricles) is a AV (meaning atrioventricular valve).  Rhythms above the ventricles are also grouped as supraventricular rhythms.  Which is what ablation is used for.

Types of rhythms a patient would be considered for ablation as a possible treatment:

Atrial fibrillation. The electrical signal that circles uncoordinated through the muscles of the atria (the upper chambers of the heart), causing them to quiver (sometimes more than 400 times per minute) without contracting. The ventricles (the lower chambers of the heart) do not receive regular impulses and contract out of rhythm, and the heartbeat becomes uncontrolled and irregular. It is the most common atrial arrhythmia, and 85 percent of people who experience it are older than 65 years.

Atrial fibrillation can cause a blood clot to form, which can enter the bloodstream and trigger a stroke. Underlying heart disease or hypertension increases the risk of stroke from atrial fibrillation as does age even without heart disease or hypertension.

Premature atrial contraction (PAC or premature atrial impulses). A common and benign arrhythmia, a PAC is a heartbeat that originates away from the sinus node, which sends electrical signals through the upper chamber. It typically occurs after the sinus node has initiated one heartbeat and before the next regular sinus discharge. A PAC can cause a feeling of a skipped heartbeat. Use of caffeine, tobacco, and/or alcohol, or stress can bring on PACs or increase their frequency.

Supraventricular tachycardia (SVT). Characterized by a rapid heart rate that ranges between 100 and 240 beats per minute, SVT usually begins and ends suddenly. SVT occurs when an electrical impulse ‘re-enters’ the atrial muscles. A disorder that a person may have at birth, SVT is commonly caused by a variation in the electrical system of the heart. SVT often begins in childhood or adolescence and can be triggered by exercise, alcohol, or caffeine. SVT is rarely dangerous, but can cause a drop in blood pressure, causing lightheadedness or near-fainting episodes, and, rarely, fainting episodes.

Atrial flutter. Differentiated from atrial fibrillation by its coordinated, regular pattern, atrial flutter is a coordinated rapid beating of the atria. Most who experience atrial flutter are 60 years and older and have some heart disorder, such as heart valve problems or a thickening of the heart muscle. Atrial flutter is classified into two types, according to the pathways responsible for it. Type I normally causes the heart rate to increase to and remain at 150 beats per minute. Rarely, the rate may reach 300 beats per minute; sometimes it decreases to 75 beats per minute. Type II increases the atrial rate faster, so the ventricular rate may be 160 to 170 beats per minute. As with atrial fibrillation, atrial flutter increases the risk of stroke.

Sick sinus syndrome (SSS). Common among older people, SSS is an improper firing of electrical impulses caused by disease or scarring in the sinus or Sinoatrial node (SA node). SSS normally causes the heart rate to slow, but sometimes it alternates between abnormally slow and fast. A progressive condition, with episodes increasing in frequency and duration, SSS can be caused by:

• Degeneration of the heart’s electrical system; or
• Diseases of the atrial muscle.

Sinus tachycardia. The sinus node emits abnormally fast electrical signals, which increases the heart rate to between 100 beats per minute to 140 beats per minute at rest, and 200 beats per minute during exercise. A normal response to exercise or stress, it can also be caused by:

• Adrenaline;
• Consumption of caffeine, nicotine, or alcohol; and
• Heart conditions.

Sinus bradycardia. Associated with impaired impulse generation in the SA node, it causes the heart rate to decrease to fewer than 60 beats per minute. Commonly caused by SSS, drugs like beta-blockers and calcium-channel blockers can also cause sinus bradycardia. Occasionally sinus bradycardia can be caused by impaired conduction of impulses to the atrial muscles.

Wolff-Parkinson-White syndrome (WPW). WPW syndrome occurs when electrical signals fail to pause in the atrioventricular node because an extra pathway allows the impulse to “bypass” the normal pathway; and the syndrome is sometimes called bypass tract. WPW syndrome causes heart rates approaching 240 beats per minute.

Occasionally, impulses can go down one extra pathway and up another, creating a “loop” or “short circuit,” (called SVT because of WPW). Patients with WPW syndrome may develop atrial fibrillation and are at increased risk for developing a dangerous ventricular arrhythmia when this occurs.

CAUSES AND RISK FACTORS

Problems with the heart’s electrical system or with the muscles’ response to the signal can cause arrhythmias. Physicians have categorized arrhythmias to their type:

• Disorders of impulse generation – A signal that generates part of the heart’s electrical system other than the SA node.
• Disorders of impulse conduction – “block” the heart’s electrical impulse and prevent it from traveling its normal pathway.
• Heart attack – causes scarring of the heart, which can interrupt electrical impulses.

People without heart disease can develop an arrhythmia for unknown causes, but risk factors can include:

• Emotional stress;
• Consumption of alcohol, caffeine, diet pills, and tobacco; and
• Some prescription medications (certain heart drugs and certain cold, cough, allergy medications and anti-depressants).

WHAT ARE THE SYMPTOMS?

The onset and duration of arrhythmia symptoms vary according to its type, frequency, duration, and whether structural heart disease is present.

Common symptoms that people experience may include:

• Palpitations (the sensation of skipped heartbeats);
• Lightheadedness;
• Shortness of breath;
• Fatigue;
• Chest pain;
• Fainting; and
• Urge to urinate.

Certain arrhythmias may cause fainting, and, occasionally stroke, while others (‘silent’ arrhythmias) cause no symptoms.

DIAGNOSIS

Arrhythmias can be difficult to diagnose because they can be unpredictable and brief. A physician will typically take a person’s medical history, and perform a physical examination, during which the physician may detect an arrhythmia using a stethoscope. Arrhythmias that occur infrequently, last for short periods of time, or do not cause noticeable symptoms may require more detailed tests, such as:

• Electrocardiogram (ECG);
• A Holter monitor (an ambulatory ECG); and/or
• A loop ECG.

Part 2 on Ablation tomorrow.

“Look at the average American diet: ice cream, butter, cheese, whole milk, all this fat. People don’t realize how much of this stuff you get by the end of the day. High blood pressure is from all this high-fat eating.”

Jack LaLanne

Factors in helping to reduce or decrease high blood pressure, also noted as hypertension are:

-STRESS REDUCTION

Stress is defined as feeling tense on the inside due to pressures from the outside. Most of us have many of these pressures, and some handle them better than others. Since stress makes the heart work harder, try to find ways to relieve the pressure you felt when stressed.

One way of coping with stress is to deal with your feelings. You may feel depressed, angry or anxious because you have high blood pressure. These feelings are normal. It may help to talk about how you feel with your family and friends. When you accept that you have high B/P, you can put your efforts into living a more productive, good life with dealing with the hypertension.

Many people find yoga, meditation and prescribed exercise helpful. Always check with your doctor before starting an exercise program to make sure you get clearance of what is safe for you by your primary doctor or cardiologist.

-Eat less SODIUM

Sodium is an important substance. It helps your body balance the level of fluid inside and outside of the cells. To keep up this balance, the body needs about 2000mg of sodium a day or less. Yet most of us eat 3000 to 6000mg of sodium each day.

Most people with high b/p are asked to eat less sodium. Sodium attracts water and makes the body hold fluid. To pump the added fluid the heart works harder. Also sodium in the body causes the arteries to vasocontrict increasing pressure in the vessels causing the pressure to rise.

Most people with high b/p are asked to eat less sodium at 2000mg or less a day and this is to prevent water retention and vasoconstriction in which both actions increase the blood pressure. Follow your doctor’s advice about your sodium intake.

Many prepared foods and spices are high in sodium. But, the most common source of sodium is table salt. Table salt is 40% sodium and 60% chloride. One teaspoon of table salt contains 2000mg of sodium.

HINTS TO LOWER YOUR SODIUM IN YOUR DIET:

-Season foods with fresh or dried herbs, vegetables, fruits or no-salt seasonings.

-Do not cook with salt or add salt to foods after they are on the table.

-Make your own breads, rolls, sauces, salad dressings, vegetable dishes and desserts when you can.

-Stay away from fast foods. They are almost all high in salt.

-Eat fresh, frozen or canned, unsalted vegetables. These have less sodium than most processed foods. Read the labels and if they don’t have a label DON’T EAT IT. Read the labels and eat the portioned size it says to for 1 portion with keeping a diary of what you ate with adding the sodium and when it reached 2000mg no more food that day with salt in it unless the doctor prescribes less.

-Buy water packed tuna and salmon. Break it up into a bowl of cold water, and let stand for 3 minutes. Rinse, drain and squeeze out water.

-Don’t buy convenience foods such as prepared or skillet dinners, deli foods, cold cuts, hot dogs, frozen entrees or canned soups. These have lots of salt. Be picky on what you eat.

-Again, read all labels for salt, sodium or sodium products (such as sodium benzoate, MSG). Ingredients are listed in the order of amount used. A low sodium label means 140mg of less per serving. Try to buy products labeled low sodium/serving. Do not eat products that have more sodium than this per serving.

-When you eat out, order baked, broiled, steamed or pouched foods without breading or butter or sauces. Also ask that no salt be added. Go easy on the salad dressing. Most are high in salt.

What not to buy:

-Canned Vegetables, sauerkraut. Self rising flour and corn meal. Prepared mixes (waffle, pancake, muffin, cornbread, etc…)

-Dairy Products- like buttermilk (store-bought), canned milks unless diluted and used as regular milk).   Egg substitute limit to ½ cup/day. Eggnog (store bought) and salted butter or margarine do not buy.

-Soups: Boullon (all kinds), canned broth, dry soup mixes, canned soups.

-Meats and meat substitutes not to buy= Canned meats, canned fish, cured meats, all types of sausages, sandwich meats, peanut butter, salted nuts.

-Prepared mixes (pie, pudding, cake) or store bought pies, cakes, muffins.

-Cooking ingredients to use low sodium type or limit to 2 tbsp/day=

Catsup, chili sauce, barbeque sauce, mustard, salad dressing.

-Drinks to stay away from Athletic Drinks (such as Gatorade), canned tomato or vegetable juice (unless unsalted).

“People with high blood pressure, diabetes – those are conditions brought about by life style. If you change the life style, those conditions will leave.”

Dick Gregory (Comedian/Social Activist born October 12, 1932.)

“SIRS can be incited by ischemia, inflammation, trauma, infection or a combination of several “insults”. SIRS is not always associated with infection. While not universally accepted, some have proposed the terms “severe SIRS” and “SIRS shock” to describe serious clinical syndromes that are not infectious in nature and thus cannot be labeled according to the various sepsis definitions”

Steven D. Burdette M.D. (Infectious Disease Medicine M.D.– Wright State Physicians in Dayton, Ohio – http://www.healthgrades.com/physician/dr-steven-burdette-yhfgy)

Part 3 talks to you about the multi-hit theory of SIRS with Inflammatory Cascade of SIRS and lastly the coagulation process in SIRS.   It also informs you of infectious and non-infections of SIRS.

Multi-hit theory

A multi hit theory behind the progression of SIRS to organ dysfunction and possibly multiple organ dysfunction syndrome (MODS). In this theory, the event that initiates the SIRS cascade primes the pump. With each additional event, an altered or exaggerated response occurs, leading to progressive illness. The key to preventing the multiple hits is adequate identification of the ETIOLOGY or CAUSE of SIRS and appropriate resuscitation and therapy.

Inflammatory cascade

Trauma, inflammation, or infection leads to the activation of the inflammatory cascade. Initially, a pro-inflammatory activation occurs, but almost immediately thereafter a reactive suppressing anti-inflammatory response occurs. This SIRS usually manifests itself as increased systemic expression of both pro-inflammatory and anti-inflammatory species. When SIRS is mediated by an infectious insult, the inflammatory cascade is often initiated by endotoxin or exotoxin. Tissue macrophages, monocytes, mast cells, platelets, and endothelial cells are able to produce a multitude of cytokines. The cytokines tissue necrosis factor–alpha (TNF-α) and interleukin-1 (IL-1) are released first and initiate several cascades.

The release of certain factors without getting into medical specific terms they ending line induces the production of other pro-inflammatory cytokines, worsening the condition.

Some of these factors are the primary pro-inflammatory mediators. In research it suggests that glucocorticoids may function by inhibiting certain factors that have been shown to be released in large quantities within 1 hour of an insult and have both local and systemic effects. In studies they have shown that certain cytokines given individually produce no significant hemodynamic response but that they cause severe lung injury and hypotension. Others responsible for fever and the release of stress hormones (norepinephrine, vasopressin, activation of the renin-angiotensin-aldosterone system).

Other cytokines, stimulate the release of acute-phase reactants such as C-reactive protein (CRP) and pro-calcitonin.

The pro-inflammatory interleukins either function directly on tissue or work via secondary mediators to activate the coagulation cascade and the complement cascade and the release of nitric oxide, platelet-activating factor, prostaglandins, and leukotrienes.

High mobility group box 1 (HMGB1) is a protein present in the cytoplasm and nuclei in a majority of cell types. In response to infection or injury, as is seen with SIRS, HMGB1 is secreted by innate immune cells and/or released passively by damaged cells. Thus, elevated serum and tissue levels of HMGB1 would result from many of the causes of SIRS.

HMGB1 acts as a potent pro-inflammatory cytokine and is involved in delayed endotoxin lethality and sepsis.

Numerous pro-inflammatory polypeptides are found within the complement cascade. It is thought they are felt to contribute directly to the release of additional cytokines and to cause vasodilatation and increasing vascular permeability. Prostaglandins and leukotrienes incite endothelial damage, leading to multi-organ failure.

Polymorphonuclear cells (PMNs) from critically ill patients with SIRS have been shown to be more resistant to activation than PMNs from healthy donors, but, when stimulated, demonstrate an exaggerated microbicidal response (agents that kill microbes). This may represent an auto-protective mechanism in which the PMNs in the already inflamed host may avoid excessive inflammation, thus reducing the risk of further host cell injury and death.

Coagulation

The correlation between inflammation and coagulation is critical to understanding the potential progression of SIRS. IL-1 and TNF-α directly affect endothelial surfaces, leading to the expression of tissue factor. Tissue factor initiates the production of thrombin, thereby promoting coagulation, and is a pro-inflammatory mediator itself. Fibrinolysis is impaired by IL-1 and TNF-α via production of plasminogen activator inhibitor-1. Pro-inflammatory cytokines also disrupt the naturally occurring anti-inflammatory mediators anti-thrombin and activated protein-C (APC).

If unchecked, this coagulation cascade leads to complications of micro-vascular thrombosis, including organ dysfunction. The complement system also plays a role in the coagulation cascade. Infection-related pro-coagulant activity is generally more severe than that produced by trauma.

What the causes of SIRS can be:

The etiology of systemic inflammatory response syndrome (SIRS) is broad and includes infectious and noninfectious conditions, surgical procedures, trauma, medications, and therapies.

The following is partial list of the infectious causes of SIRS:

• Bacterial sepsis
• Burn wound infections
• Candidiasis
• Cellulitis
• Cholecystitis
• Community-acquired pneumonia ^[5]
• Diabetic foot infection
• Erysipelas
• Infective endocarditis
• Influenza
• Intra-abdominal infections (eg, diverticulitis, appendicitis)
• Gas gangrene
• Meningitis
• Nosocomial pneumonia
• Pseudomembranous colitis
• Pyelonephritis
• Septic arthritis
• Toxic shock syndrome
• Urinary tract infections (male and female)

The following is a partial list of the noninfectious causes of SIRS:

• Acute mesenteric ischemia
• Adrenal insufficiency
• Autoimmune disorders
• Burns
• Chemical aspiration
• Cirrhosis
• Cutaneous vasculitis
• Dehydration
• Drug reaction
• Electrical injuries
• Erythema multiform
• Hemorrhagic shock
• Hematologic malignancy
• Intestinal perforation
• Medication side effect (ex. from theophylline)
• Myocardial infarction
• Pancreatitis
• Seizure
• Substance abuse – Stimulants such as cocaine and amphetamines
• Surgical procedures
• Toxic epidermal necrolysis
• Transfusion reactions
• Upper gastrointestinal bleeding
• Vasculitis

PREVENTION IS THE KEY!   So stay healthy and out of  hospitals!*

The treatment is don’t get it since it is hard to get rid of especially the people over 65 and in hospitals.  There is no one Rx for it.  If your unfortunate enough to be diagnosed with SIRS the sooner you get diagnosed with it including being in stage one as opposed to three the better the turn out will be for you.  Again the key is prevention; don’t get it.

It is the body’s response to an infectious or noninfectious insult. Although the definition of Systemic Inflammatory Response Syndrome (SIRS) refers to it as an “inflammatory” response, it actually has pro- and anti-inflammatory components.  SIRS is a serious condition related to systemic inflammation, organ dysfunction, and organ failure. It is a subset of cytokine storm, in which there is abnormal regulation of various cytokines.   Cytokines are this, the term “cytokine” is derived from a combination of two Greek words – “cyto” meaning cell and “kinos” meaning movement. Cytokines are cell messaging or signaling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma.

Cytokines exist in peptide, protein and glycoprotein (proteins with a sugar attached) forms. The cytokines are a large family of molecules that are classified in various different ways due to an absence of a unified classification system.  Protein is acidic as opposed to being alkalinic.

Examples of cytokines include the agents interleukin and the interferon which are involved in regulating the immune system’s response to inflammation and infection.

SIRS, independent of the etiology/cause, has the same pathophysiologic properties, with minor differences in inciting cascades. Many consider the syndrome a self-defense mechanism. Inflammation is the body’s response to nonspecific insults that arise from chemical, traumatic, or infectious stimuli. The inflammatory cascade is a complex process that involves humoral and cellular responses, complement, and cytokine cascades.  Best summarized in the relationship between these complex interactions and SIRS is it is in the following 3-stage process.  Here is a simple explanation in what occurs without taking pages in explaining the stages.

Stage I

Following an insult to the body, cytokines are produced at the site. Local cytokine production incites an inflammatory response, thereby promoting wound repair and recruitment of the reticular endothelial system. This process is essential for normal host defense homeostasis and if absent is not compatible with life. Local inflammation, such as in the skin and subcutaneous soft tissues occurs.

What occurs is rubor or redness at the site that reflects local vasodilation of vessels.  What is caused by release of local vasodilation of the vessels at the area of where the insult starts in the body is substances like nitric oxide (NO) and prostacyclin get released=Acidic.

Tumor or swelling occurs due to vascular endothelial (layer of the skin) tight junction disruption and the local extravasation of protein-rich fluid into the interstitium (layer of the skin), which also allows activated white blood cells to pass from the vascular space (blood stream) into the tissue space to help clear infection and promote repair.

Dolor is pain and represents the impact inflammatory mediators have on local somatosensory nerves. Presumably, this pain stops the host from trying to use this part of his or her body as it tries to repair itself.

The increased heat primarily due to increased blood flow occurs but also increased local metabolism as white blood cells become activated and localize to the injured tissue.

Finally, the loss of function, a hallmark of inflammation and a common clinical finding of organ dysfunction with the infection is isolated to a specific organ (ex. pneumonia—acute respiratory failure; kidney—acute kidney injury. pancreatitis–  inflammation of the pancreas).

Importantly, on a local level, this cytokine and chemokine release by attracting activated leukocytes to the region may cause local tissue destruction (ex. abscess) or cellular injury (ex. pus), which appear to be the necessary byproducts of an effective local inflammatory response.  Local infection signs & symptoms= puss, swelling. skin temperature  hot, pain and redness to the where the insult of the body is.

Ending line what happens is an insult occurs in the body, there is local cytokine production with the goal of inciting an inflammatory response thereby promoting wound repair and recruitment of the reticular endothelial system.  Your body is compensating in reacting normally to this insult.

Stage II

Small quantities of local cytokines are released into the circulation, improving the local response. This leads to growth factor stimulation and the recruitment of macrophages and platelets. This acute phase response is typically well controlled by a decrease in the pro-inflammatory mediators and by the release of endogenous antagonists; the goal is homeostasis. At this stage, some minimal malaise (general weakness)and low-grade fever may become show.

Putting it simple what occurs here is small quantities of local cytokines are released into circulation to improve the local response. This leads to growth factor stimulation and the recruitment of macrophages (cells eating up toxins to the body) and platelets (that are cells the coagulate-cause clotting). This acute phase response is typically well controlled by a decrease in the proinflammatory mediators and by the release of endogenous antagonists. The goal is homeostasis – the body still trying to compensate and react productively to this insult to the body.

Stage III

If homeostasis is not restored and if the inflammatory stimuli continue to seed into the systemic circulation, a significant systemic reaction occurs. The cytokine release (acidic) leads to destruction rather than protection. A consequence of this is the activation of numerous humoral cascades and the activation of the reticular endothelial system and subsequent loss of circulatory integrity.  The body at this stage is decompensating and not productively fighting off this insult to the body and this leads to end-organ dysfunction.

Tune in tomorrow to part 3 of SIRS the conclusion of this topic (extensive noninfectious and infectious causes with more on coagulation and multi cascading reactions in the body due to SIRS).