Biologic Crisis:

Pathophysiologic Mechanism of Cardiac failure, Acute Myocardial Infarction, Acute Respiratory Failure, Acute Renal Failure, Stroke, Increased Intracranial Failure, Metabolic Emergencies: DKA, and HHNS

Prepared by: Recitas, Anna Lou G. BSN-4 SN-DOSCST

Cardiac Failure
Cardiac failure is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. It is often referred to as Congestive Heart Failure (CHF) and characterized by signs and symptoms of fluid overload or of inadequate tissue perfusion. Fluid overload and tissue perfusion result when the heart cannot generate a cardiac output sufficient to meet the bodys demands.

Systolic heart failure

Systolic heart failure is the result of a pumping problem (systolic dysfunction), caused by the ventricle losing its ability to contract normally because the heart muscle has become weak. When this happens, the heart can't pump with enough force and not enough blood is pushed into the circulation.

Diastolic heart failure

Diastolic heart failure is the result of a filling problem (diastolic dysfunction), caused by the ventricle losing its ability to relax normally because the heart muscle has become stiff. When this happens, the heart can't fill with enough blood, resulting in too little blood being pumped back out into the circulation.

Left-sided heart failure

The most common causes of leftsided heart failure are acute MI and cardiomyopathy. Pulmonary congestion occurs when the left ventricle cannot effectively pump out the ventricle into the aorta and the systemic circulation. Stenosis and regurgitation of the aortic or mitral valves also creates the level of leftsided backflow that results in pulmonary congestion.

Right-sided heart failure

The right side of the heart cannot eject blood and cannot accommodate all the blood that returns to it from the venous circulation. When the heart ventricle fails, congestion in the peripheral tissues and the viscera predominates. The causes of right-sided heart failure include conditions that restrict blood flow into the lungs. Stenosis or regurgitation of the tricuspid or pulmonic valves, right ventricular infarction, cardiomyopathy, and persistent left-sided failure are common cause. As the heart's pumping action is lost, blood may back up in other areas of the body, causing fluid to build up in the lungs, the liver, the gastrointestinal tract, and the arms and legs.

Right-sided heart failure

Left-sided heart failure

Congestion of peripheral tissues

Decreased cardiac output

Pulmonary congestion

Dependent edema and ascites

Liver congestion

Activity intolerance and signs of decreased tissue perfusion

Impaired gas exchange

Pulmonary edema

Cyanosis and signs of hypoxia

GI tract congestion

Signs related to impaired liver function: hepatomegaly ; right-upper quadrant pain

Cough with frothy sputum Orthopnea Paroximal nocturnal dyspnea

Anorexia, GI distress, weight loss

Pathophysiology
Causes: Myocardial infarction Hypertension Coronary heart disease Valve disease Ischemic heart disease hyperthyroidism

Reduced blood flow

Decreased perfusion to kidneys

Decreased cardiac output Decreased systemic blood pressure

Activation of renninangiotensin-aldosterone system

Activation of baroreceptors Left ventricle Aortic arch Carotid sinus

Kidney release renin

Renin acts on the blood protein angiotensinogen, angiotensin 1 is produced

Stimulation of vasomotor regulatory centers in medulla

Angiotensin 1 converted to Angiotensin 2 by ACE

Activation of sympathetic nervous system

Increase catecholamine (Epinephrine and norepinephrine)

Ventricular remodeling Hypertrophy and dilatation of ventricle Large cells Impaired contractility

Aldolsterone Sodium and water retension Vasopressin endothelin

Vasoconstriction afterload blood pressure heart rate

Acute Myocardial Infarction

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack is the interruption of blood supply to a part of the heart, causing heart cells to die. It occurs when the blood supply to part of the heart is interrupted. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (like cholesterol) and white blood cells (especially macrophages) in the wall of an artery.

Causes of AMI
Heart attacks most often occur as a result of coronary heart disease (CHD), also called coronary artery disease. CHD is a condition in which a waxy substance called plaque (plak) builds up inside the coronary arteries. These arteries supply oxygenrich blood to your heart. When plaque builds up in the arteries, the condition is called atherosclerosis. The buildup of plaque occurs over many years. Eventually, an area of plaque can rupture (break open) inside of an artery. This causes a blood clot to form on the plaque's surface. If the clot becomes large enough, it can mostly or completely block blood flow through a coronary artery. If the blockage isn't treated quickly, the portion of heart muscle fed by the artery begins to die. Healthy heart tissue is replaced with scar tissue. This heart damage may not be obvious, or it may cause severe or long-lasting problems.

A less common cause of heart attack is a severe spasm (tightening) of a coronary artery. The spasm cuts off blood flow through the artery. Spasms can occur in coronary arteries that aren't affected by atherosclerosis. Heart attacks can be associated with or lead to severe health problems, such as heart failure and lifethreatening arrhythmias.

Common causes of AMI

Common signs and symptoms of a heart attack include new onset of:
Upper body discomfort in one or both arms, the back, neck, jaw, or upper part of the stomach Shortness of breath, which may occur with or before chest discomfort Nausea (feeling sick to your stomach), vomiting, light-headedness or sudden dizziness, or breaking out in a cold sweat Sleep problems, fatigue (tiredness), or lack of energy

Acute Respiratory Failure

It is a sudden and life-threatening deterioration of the gas exchange function of the lung. It is also defined as a decrease in arterial oxygen tension (PaO) to less than 50 mmHg (hypoxemia) and an increase in arterial Carbon Dioxide tension (PaO) to greater than 50 mmHg (hypercapnia), with an arterial h of less than 7.35.

Causes:
Impaired ventilation (hypoventilation) It occurs when the volume of fresh air moving in and out of the lung is significantly reduced. It is commonly caused by conditions outside the lung such as: Depression of the respiratory center (e.g., drug abuse) Disease of the nerve supplying the respiratory muscles (e.g., Guillain-Barr Syndrome) Disorders of the respiratory muscles (e.g., muscular dystrophy) Upper airway obstruction such as infection (e.g., epiglottitis), foreign body, laryngospasm and tumors.

Ventilation-Perfusion Mismatching Shunt -there is a perfusion without ventilation - refers to blood that moves from the right to the left side of the circulation without being oxygenated -occurs in conditions such as atelectasis in which there is airway obstruction Dead air space -there is ventilation without perfusion -refers to the volume to the volume of air that must be moved with each breath but does not participate in gas exchange -occurs in conditions such as pulmonary embolism which impairs blood flow to the a part of the lung

Impaired diffusion It describes a condition in which gas exchange between the alveoli and red blood cells is impeded because of an increase in the distance or a decrease in the permeability of the alveolar capillary membrane to movement of gas. It is commonly occurs in conditions such as interstitial lung disease, ARDS, pulmonary edema and pneumonia.

Hypoventilation, mismatching of ventilation and perfusion and impaired diffusion will result to hypoxemia and hypercapnia.

Hypoxemia This refers to a reduction in blood oxygen levels. The mechanisms whereby respiratory disorders lead to a significant reduction in PO2 are hypoventilation, impaired diffusion of gases, shunt and mismatching of ventilation and perfusion. Hypoxemia produces its effect through tissue hypoxia and the compensatory mechanism that the body uses to adapt to the lowered oxygen

Hypercapnia This refers to an increase in the carbon dioxide content of the arterial blood. Caused by hypoventilation or mismatching of perfusion and diffusion.

Pathophysiology
COPD
Depression of the respiratory center (drug overdose) Guillain-Barr Syndrome) muscular dystrophy infection, foreign body, laryngospasm and tumors

Pulmonary edema Pneumonia

Ventilationperfusion mismatching

hypoventilation

Impaired diffusion

hypercapnia

hypoxemia

hypercapnia

hypoxemia
pH

vasodilation Sedative effect on the nervous system

Tissue hypoxia in cerebral edema Respiratory acidosis Anaerobic metabolism takes place

cerebral flow Headache, warm and flushed skin

Carbon dioxide narosis

Progressive disorientation Somnolence

Release of lactic acid

Loss of consciousness

coma
death

Manifestations
Mild hypoxia: Slight impairment of mental performance Visual acuity Sometimes hyperventilation More pronounced hypoxemia Personality changes Restless Agitated Uncoordinated muscle movement Euphoria Impaired judgment Delirium Stupor and coma Cyanosis- late sign of respiratory failure -marked in the lips, nail beds, ears and cheeks.

Acute Renal Failure

Acute Renal Failure is a reversible clinical syndrome where there is a sudden and almost complete loss of kidney function (decrease GFR) over a period of hours to days with failure to excrete nitrogenous waste products and to maintain fluid and electrolyte homeostasis (Porth, 2005).

Prerenal failure
It is the most common form of acute renal failure, is characterized by marked decrease in renal blood flow. It is reversible if the cause of the decreased renal blood flow can be identified and corrected before kidney damage occurs. Prerenal failure refers to any disruption on the cardiovascular side of the nephron. Specifically, anything that originates in the circulatory blood supply of the nephron that impairs its function.

Cause of Prerenal failure

Left-Sided Heart Failure. Heart failure is a condition in which cardiac output is insufficient to meet body needs. One of those needs in systemic circulation is adequate kidney perfusion to keep filtration function and waste removal within normal limits. Admittedly, with left CHF blood backs up into the lungs causing respiratory problems. But, it is the diminished output into the aorta from the failing heart that lowers kidney perfusion downstream and can result in renal failure with its associated low urine output and accumulation of wastes in circulating blood and body fluids.

Cause of Prerenal failure

Glomerulonephritis. In this condition, antibody complexes resulting from a recent infection collect on the glomerular membrane on the circulatory side and cause a secondary glomerular inflammation. This glomerular inflammation can cause permanent nephron damage by fibrous connective tissue infiltration which interferes with the glomerular filtration process. Streptococcal infections are notorious as causative agents of acute glomerulonephritis. Consequently, something as simple as a strep throat can have serious consequences.

Cause of Prerenal failure

Chronic Hypertension and Benign Nephrosclerosis. Because of the large number of small diameter blood vessels associated with the kidney, kidney function is extremely sensitive to high blood pressure. Elevated pressures can cause blood vessel damage as plasma leaks into the artery wall under pressure. This plasma infiltration begins an inflammatory response that thickens the artery walls with resultant renal ischemia. Renal ischemia, in turn, can further damage the kidney.

Postrenal failure
It results from obstruction of urine outflow from the kidneys. The obstruction occurs in the ureter, bladder, or urethra. Postrenal failure is sometimes referred to as obstructive renal failure, since it is often caused by something blocking elimination of urine produced by the kidneys. It is the rarest cause of acute kidney failure (5%-10% of all cases).

Causes of Postrenal failure

Renal Calyx (Kidney Stone). Kidney stones result from crystalline materials that

occur in urine in concentrations sufficient to cause aggregate crystals that grow into stones within the renal pelvis. Once formed, these stones can move into the ureters and lodge causing intense pain until they are passed naturally or are removed surgically or disrupted by ultrasound treatments. A common kidney stone develops from calcium oxylate salts in people with high calcium and oxalic acid in their diets. Calcium comes primarily from dairy products and leafy green vegetables, both of which are common in southern diets. Oxylates come from plant extracts (coffee, tea, and cola), which are also common in southern diets.

Causes of Postrenal failure

Pyelonephritis. Pyelonephritis is a condition which develops when infectious microorganisms establish in the urinary tract and migrate upward into kidney tissue. The incidence is particularly high in individuals who contaminate the urethra with fecal material containing E. coli as a result of poor hygiene or are unable to completely void the bladder for some reason. The urinary retention leads to excess microbial growth and eventual spread into the kidneys.

Causes of Postrenal failure

Obstruction of one or both ureters can be caused by the following: Cancer of the urinary tract organs or structures near the urinary tract that may obstruct the outflow of urine Obstruction at the bladder level can be caused by the following: Bladder stone Enlarged prostate (the most common cause in men) Blood clot Bladder cancer

Intrinsic or Intrarenal failure

It results from conditions can cause damage to structures within the kidney- glomerular, tubular or interstitial. The major cause of intrarenal failure are toxic insults to the tubular structures of the nephron and intratubular obstruction.

Causes of Intrarenal failure

Toxins (Acute Tubular Necrosis, ATN) Many bacteria, especially certain strains of Escherichia coli, secrete toxic materials that can be damaging to the host. In humans, these toxins may exist in circulating blood at levels too low to cause problems until they are filtered into the nephron across the glomerulus. Once filtered into the nephron, tubular reabsorption results in these toxins being concentrated in the nephron, eventually reaching a concentration high enough to damage nephron tubule cells (tubular necrosis).

Acute Kidney Failure Symptoms

The following symptoms may occur with acute kidney failure. Some people have no symptoms, at least in the early stages. The symptoms may be very subtle. Decreased urine production Body swelling Problems concentrating Confusion Fatigue Lethargy Nausea, vomiting Diarrhea Abdominal pain Metallic taste in the mouth Seizures and coma may occur in very severe acute kidney failure

Cerebrovascular accident or Stroke

Cerebrovascular accident or stroke (also called brain attack) results from sudden interruption of blood supply to the brain, which precipitates neurologic dysfunction lasting longer than 24 hours. Stroke are either ischemic, caused by partial or complete occlusions of a cerebral blood vessel by cerebral thrombosis or embolism or hemorrhage (leakage of blood from a vessel causes compression of brain tissue and spasm of adjacent vessels).

ISCHEMIC STROKE
Ischemic stroke occurs when a blood vessel that supplies blood to the brain is blocked by a blood clot. This may happen in two ways: A clot may form in an artery that is already very narrow. This is called a thrombus. If it completely blocks the artery, it is called a thrombotic stroke. A clot may break off from another place in the blood vessels of the brain, or some other part of the body, and travel up to the brain to block a smaller artery. This is

Ischemic strokes may result from clogged arteries, a condition called atherosclerosis. This may affect the arteries within the brain or the arteries in the neck that carry blood to the brain. Fat, cholesterol, and other substances collect on the wall of the arteries, forming a sticky substance called plaque. Over time, the plaque builds up. This often makes it hard for blood to flow properly, which can cause the blood to clot.

Ischemic strokes may also be caused by blood clots that form in the heart or other parts of the body. These clots travel through the blood and can get stuck in the small arteries of the brain. This is known as a cerebral embolism.

ISCHEMIC STROKE

HEMORRHAGIC STROKE
Hemorrhagic stroke occurs when a blood vessel in part of the brain becomes weak and bursts open, causing blood to leak into the brain. Some people have defects in the blood vessels of the brain that make this more likely. The flow of blood that occurs after the blood vessel ruptures damages brain cells.

Increased Intracranial Pressure

Increased ICP is a life threatening situation that results from an increased in any of all the three components (brain tissue, blood and CSF) of the skull. Cerebral edema is an important factor contributing to increase ICP). Increased Intracranial pressure is the common pathway for brain injury from different types of insults and agents. Excessive ICP can obstruct cerebral blood flow, destroy brain cells, displaced brain tissue as in herniation and otherwise damage delicate brain structures

Causes of Increased Intracranial Pressure

Causes of increased intracranial pressure include serious diseases and conditions, such as hydrocephalus, which is an increase in the volume of cerebrospinal fluid that surrounds the brain and spinal cord. Increased intracranial pressure can also be due to diseases or conditions that create abnormally high pressure within the skill, such as a brain tumor or swelling of brain tissue due to encephalitis, an inflammation of the brain often caused by a viral infection. Increased intracranial pressure can also be caused by bleeding into or on the brain due to such conditions as a serious head injury or hemorrhagic stroke.

Symptoms of increased intracranial pressure may include lethargy, vomiting, seizures, vision changes, and behavior changes. The headache that may occur with increased intracranial pressure is often described as the worst headache of my life.

Cranial insult

Tissue edema

Compression of blood vessels

cerebral blood flow

Oxygen with death of brain cells Edema around the necrotic tissue

ICP with compression of brainstem and respiratory center

Accumulation of carbon dioxide

vasodilation

ICP resulting from blood flow

death

Diabetic ketoacidosis (DKA)

DKA is a complication of diabetes that occurs when the body cannot use sugar (glucose) as a fuel source because the body has no insulin or not enough insulin, and fat is used instead. Byproducts of fat breakdown, called ketones, build up in the body. The three major derangements in DKA are hyperglycemia (blood glucose levels >250 mg/dL), ketosis and metabolic acidosis (low serum bicarbonate [<15 mEq/L] and low pH [<7.3]).

It is most commonly occurs in a person with type 1 diabetes mellitus, in whom the lack of insulin leads to mobilization of fatty acids from adipose tissue because of the unsuppressed adipose cell lipase activity that breaks down triglycerides into fatty acids and glycerol. The increase in fatty acid levels leads to ketone production by the liver.

Lack of insulin

Decreased utilization of glucose by muscles, fat, and liver Increased production of glucose by liver

Increased breakdown of fat

Increased fatty acids

hyperglycemia

Increased ketone bodies (acetone breath, poor appetite, nausea) Osmotic diuresis (polyuria; water, electrolyte loss)

Blurred vision

Metabolic acidosis (nausea, vomiting, abdominal pain)

Dehydration (weakness, headache)

Increrasingly rapid respirations

Increased thirst (polydipsia)

CNS depression

Circulatory failure

coma

Hyperosmolar Hyperglycemic Nonketotic state (HHNS)

Hyperosmolar hyperglycemic state characterized by hyperglycemia (blood glucose > 600 mg/ dL), hyperosmolarity (plasma osmolarity > 310 mOsm/L) and dehydration, the absence of ketoacidosis, and depression of the sensorium.

Causes of HHNS
HHNS may occur in various conditions, including type 2 diabetes, acute pancreatitis, severe infection, MI, and treatment of oral or parenteral nutrition solutions. Two factors appear to contribute to the hyperglycemia: resistance to the effects of insulin and an excessive carbohydrate intake.

Pathophysiology
HHNS is associated with severe elevations in the blood glucose level, often exceeding 600 mg/dL, from an absolute or relative insulin deficiency or from a decreased response of the tissue to the circulating insulin (insulin resistance). This results in glycogenolysis, gluconeogenesis, and a decreased uptake of glucose by the peripheral tissue. A decline in renal function, which is typically found in the elderly patient or in patients with renal disease, also contributes to a decrease in glucose clearance. Glycogenolysis may have a limited contribution to the hyperglycemic state since many of the patients are debilitated or suffer from an acute illness and have a poor diet as a result, causing the glycogen stores in the liver to deplete over time.

The elevated blood glucose level creates a hyperosmolar extracellular space that begins to pull fluid and dehydrate the intracellular space. Initially, this influx of fluid will maintain the blood pressure and perfusion. Once the blood glucose level exceeds 180 to 250 mg/dL, a significant amount of glucose will spill into the urine. As the osmotic diuresis continues, the intravascular volume is profoundly depleted, which further decreases renal perfusion and the ability of the kidneys to remove glucose from the blood. The average fluid loss is typically 9 to ten liters in a 70 kg patient. A common cause of death is circulatory collapse.

The change in the serum osmotic pressure may cause potassium, sodium, chloride, phosphate, magnesium and bicarbonate to be depleted from the tissues, even though the serum electrolyte levels may appear to be normal or elevated. Sodium, potassium, phosphate and magnesium are typically lost during the osmotic diuresis leading to electrolyte imbalances.

Unlike DKA, the patient with HHNS does not develop ketoacidosis. There are many theories as to why there is a lack of ketogenesis; however, the exact cause is not well understood. It is thought that the continued secretion and availability of small amounts of insulin decreases the mass release of counter-regulatory hormones and reduces the availability of free fatty acids needed to produce ketones. With no ketoacidosis, the patient will not present with Kussmauls respirations or a fruity (acetone) odor on the breath.

Signs and Symptoms

The clinical presentation of HHNS is related to volume depletion and dehydration with a slow onset of signs and symptoms, usually progressing over a few days. In the early phase of HHNS, the signs and symptoms may be vague such as leg cramps, weakness and visual disturbances. As the blood glucose level continues to increase and the patient further dehydrates, the signs and symptoms usually progress in severity to include an alteration in mental status. Other signs and symptoms include: Thirst Fever (may suggest sepsis or infection as the predisposing factor) Polyuria (early) Oliguria (often a late sign of a severe dehydrated state) Drowsiness, confusion, lethargy, or coma Focal seizures that may be continuous (epilepsia partialis continua) or intermittent

Generalized seizures Hemiparesis or sensory deficits Tachycardia Orthostatic hypotension Hypotension (late signs of profound dehydration) Poor skin turgor (not a reliable sign in the elderly) Dry skin and mucous membranes Sunken eyes Excessively elevated blood glucose level

Extreme hyperglycemia

Severe osmotic diuresis

Fluid volume deficit

sodium

potassium

phosphorus

Electrolyte imbalance

Profound dehydration

hyperosmolarity

hypovolemia

 renal perfusion

hypotension

hemoconcentration

oliguria

Tissue hypoxia Lactic acid

hyperviscosity

thrombosis anuria

Seizures Shock Coma death