MS Nursing Lecture

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Information about MS Nursing Lecture

Published on August 19, 2008

Author: internist69

Source: slideshare.net

Description

discussion for the nurses' review regards the medical surgical problems in relation to the nursing practice

rsm, md

Dr. Ronald Sanchez – Magbitang EDUCATIONAL ATTAINMENT NEHS UST – B.S. Biology (Pre-Med) SLU – Doctor of Medicine (“Meritus”) TRAININGS Dr. PJGMRMC – Internal Medicine Children's Medical Center – Hematology RITM – 1 st In-Country Training in HIV AIDS PCP Symposium and Conventions PHA Conventions PRESENT POSITION Chief of Hospital Gov. Eduardo L. Joson Memorial Hospital Daan Sarile, Cabanatuan City

EDUCATIONAL ATTAINMENT

NEHS

UST – B.S. Biology (Pre-Med)

SLU – Doctor of Medicine

(“Meritus”)

TRAININGS

Dr. PJGMRMC – Internal Medicine

Children's Medical Center – Hematology

RITM – 1 st In-Country Training in HIV AIDS

PCP Symposium and Conventions

PHA Conventions

PRESENT POSITION

Chief of Hospital

Gov. Eduardo L. Joson Memorial Hospital

Daan Sarile, Cabanatuan City

PRE - TEST Primary symptom complained by patients with myocardial infarction … Normal BP is below… mmHg Aneurysm is due to the weakness of the blood vessel walls of veins… True or False? The different cardiac valves are…. The AV and semilunar valves The normal physiologic pacemaker of the heart is the… The heart has two sides, with 2 chambers left and right… True or False? Different categories of stroke according to time course, are… Endocrine system functions is primarily controlled by this gland Atrophy of the brain is noted in Alzheimer’s… True or False? TNM classification is used in what type of ailments?

Primary symptom complained by patients with myocardial infarction …

Normal BP is below… mmHg

Aneurysm is due to the weakness of the blood vessel walls of veins… True or False?

The different cardiac valves are…. The AV and semilunar valves

The normal physiologic pacemaker of the heart is the…

The heart has two sides, with 2 chambers left and right… True or False?

Different categories of stroke according to time course, are…

Endocrine system functions is primarily controlled by this gland

Atrophy of the brain is noted in Alzheimer’s… True or False?

TNM classification is used in what type of ailments?

PRE - TEST ECG means… EEG means… EMG means… CT scan means… MRI means… PET means… LP means… CSF means… FEV means… RIND and TIA means…

ECG means…

EEG means…

EMG means…

CT scan means…

MRI means…

PET means…

LP means…

CSF means…

FEV means…

RIND and TIA means…

 

Medical – Surgical Nursing CARDIOVASCULAR Myocardial Infarction Cardiac Anomalies Valvular Heart Disease Cardiac Conduction Problems Hypertension Aneurysm DVT Neurology Cerebro-vascular Accident Myasthenia Gravis Multiple Sclerosis Guillain Barre Syndrome Parkinson’s Disease Alzheimer’s Disease Huntington’s Chorea RESPIRATORY Bronchial Asthma COPD – Bronchitis & Emphysema Pneumonia ENDOCRINE Cushing’s Disease Hypothyroidism / Hyperthyroidism Diabetes Insipidus Diabetes Mellitus Grave’s Disease 0NCOLOGY EENT Meniere’s Disease Glaucoma Cataract INTEGUMENTARY / SKIN / DERMATOLOGY GASTROENTEROLOGY Liver Cirrhosis RENAL / NEPHROLOGY Renal Failure – Acute, Chronic, ESRD Dialysis – Peritoneal, Hemodialysis GENITO-URINARY / UROLOGY MUSCULOSKELETAL Arthritis HEMATOLOGY Leukemia

CARDIOVASCULAR

Myocardial Infarction

Cardiac Anomalies

Valvular Heart Disease

Cardiac Conduction Problems

Hypertension

Aneurysm

DVT

Neurology

Cerebro-vascular Accident

Myasthenia Gravis

Multiple Sclerosis

Guillain Barre Syndrome

Parkinson’s Disease

Alzheimer’s Disease

Huntington’s Chorea

RESPIRATORY

Bronchial Asthma

COPD – Bronchitis & Emphysema

Pneumonia

ENDOCRINE

Cushing’s Disease

Hypothyroidism / Hyperthyroidism

Diabetes Insipidus

Diabetes Mellitus

Grave’s Disease

THE HEART

How the Heart Works The heart has two sides, separated by an inner wall called the septum . The right side of the heart pumps blood to the lungs to pick up oxygen. Then, oxygen-rich blood returns from the lungs to the left side of the heart, and the left side pumps it to the body. The heart has four chambers and four valves , and it is connected to various blood vessels. Veins are the blood vessels that carry blood from the body to the heart, while arteries are the vessels that carry blood away from the heart to the body.

The heart has two sides, separated by an inner wall called the septum . The right side of the heart pumps blood to the lungs to pick up oxygen. Then, oxygen-rich blood returns from the lungs to the left side of the heart, and the left side pumps it to the body.

The heart has four chambers and four valves , and it is connected to various blood vessels. Veins are the blood vessels that carry blood from the body to the heart, while arteries are the vessels that carry blood away from the heart to the body.

Heart Chambers The heart has four chambers or "rooms"—two on the left side of the heart and two on the right. The atria (AY-tree-uh) are the two upper chambers that collect blood as it comes into the heart. The ventricles are the two lower chambers that pump blood out of the heart to the lungs or other parts of the body

Heart Chambers

The heart has four chambers or "rooms"—two on the left side of the heart and two on the right.

The atria (AY-tree-uh) are the two upper chambers that collect blood as it comes into the heart.

The ventricles are the two lower chambers that pump blood out of the heart to the lungs or other parts of the body

Heart Valves Four valves control the flow of blood from the atria to the ventricles and from the ventricles into the two large arteries connected to the heart. The four valves are: The tricuspid (tri-CUSS-pid) valve is in the right side of the heart, between the right atrium and the right ventricle. The pulmonary valve is in the right side of the heart, between the right ventricle and the entrance to the pulmonary artery that carries blood to the lungs. The mitral (MI-trul) valve is in the left side of the heart, between the left atrium and the left ventricle. The aortic (ay-OR-tik) valve is in the left side of the heart, between the left ventricle and the entrance to the aorta, the artery that carries blood to the body. Valves are like doors that open and close. They open to allow blood to flow through to the next chamber or to one of the arteries, and then they shut to keep blood from flowing backwards. When your heart's valves open and close, they make the familiar "lub-DUB" or "lub-DUPP" sounds that your doctor can hear by using a stethoscope. The first sound is made by the tricuspid and mitral valves closing at the beginning of systole (SIS-toe-lee). Systole is when the heart contracts, or squeezes, and pumps blood out of the heart. The second sound is made by the aortic and pulmonary valves closing at the beginning of diastole (di-AS-toe-lee). Diastole is when the heart relaxes and fills with blood.

Heart Valves

Four valves control the flow of blood from the atria to the ventricles and from the ventricles into the two large arteries connected to the heart.

The four valves are:

The tricuspid (tri-CUSS-pid) valve is in the right side of the heart, between the right atrium and the right ventricle.

The pulmonary valve is in the right side of the heart, between the right ventricle and the entrance to the pulmonary artery that carries blood to the lungs.

The mitral (MI-trul) valve is in the left side of the heart, between the left atrium and the left ventricle.

The aortic (ay-OR-tik) valve is in the left side of the heart, between the left ventricle and the entrance to the aorta, the artery that carries blood to the body.

Valves are like doors that open and close. They open to allow blood to flow through to the next chamber or to one of the arteries, and then they shut to keep blood from flowing backwards.

When your heart's valves open and close, they make the familiar "lub-DUB" or "lub-DUPP" sounds that your doctor can hear by using a stethoscope.

The first sound is made by the tricuspid and mitral valves closing at the beginning of systole (SIS-toe-lee). Systole is when the heart contracts, or squeezes, and pumps blood out of the heart.

The second sound is made by the aortic and pulmonary valves closing at the beginning of diastole (di-AS-toe-lee). Diastole is when the heart relaxes and fills with blood.

Arteries The arteries are the major blood vessels connected to your heart. The pulmonary artery carries blood pumped from the right side of the heart to the lungs to pick up a fresh supply of oxygen. The aorta is the main artery that carries oxygen-rich blood pumped from the left side of the heart out to the body. The coronary arteries are the other important arteries attached to the heart. They carry oxygen-rich blood to the heart muscle, which must have its own blood supply to function. Veins The veins are major blood vessels connected to your heart. The pulmonary veins carry oxygen-rich blood from the lungs to the left side of the heart so the blood can be pumped out to the body. The vena cava is a large vein that carries oxygen-poor blood from the body back to the heart.

Arteries

The arteries are the major blood vessels connected to your heart.

The pulmonary artery carries blood pumped from the right side of the heart to the lungs to pick up a fresh supply of oxygen.

The aorta is the main artery that carries oxygen-rich blood pumped from the left side of the heart out to the body.

The coronary arteries are the other important arteries attached to the heart. They carry oxygen-rich blood to the heart muscle, which must have its own blood supply to function.

Veins

The veins are major blood vessels connected to your heart.

The pulmonary veins carry oxygen-rich blood from the lungs to the left side of the heart so the blood can be pumped out to the body.

The vena cava is a large vein that carries oxygen-poor blood from the body back to the heart.

 

MYOCARDIAL INFARCTION Myocardial Infarction – refers to the process by which the myocardial/ cardiac tissue is destroyed in the region of the heart that are deprived of an adequate blood supply (reduced coronary artery blood flow) Causes/Etiologies: - narrowing or complete occlusion of coronary artery - decreased coronary blood flow - increased demand for oxygen Myocardial Infarction maybe defined by the location of the injury to the heart muscle or by the point in time in the process of infarction

Risk factors for atherosclerosis are generally risk factors for myocardial infarction: older age male gender[ citation needed ] cigarette smoking hypercholesterolemia (more accurately hyperlipoproteinemia , especially high low density lipoprotein and low high density lipoprotein ) diabetes (with or without insulin resistance ) high blood pressure Obesity (defined by a body mass index of more than 30 kg/m2, or alternatively by waist circumference or waist-hip ratio ). Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile. Non-modifiable risk factors include age, gender, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI. To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.

Risk factors for atherosclerosis are generally risk factors for myocardial infarction:

older age

male gender[ citation needed ]

cigarette smoking

hypercholesterolemia (more accurately hyperlipoproteinemia , especially high low density lipoprotein and low high density lipoprotein )

diabetes (with or without insulin resistance )

high blood pressure

Obesity (defined by a body mass index of more than 30 kg/m2, or alternatively by waist circumference or waist-hip ratio ).

Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile. Non-modifiable risk factors include age, gender, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition

Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI. To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status

Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.

Clinical Manifestation Chest pain – may radiate to the jaw, neck, shoulders, and arm (usually left) Pain may be accompanied by cool skin, pallor, clammy diaphoresis, tachycardia, and tachypnea Patients with DM may not experience severe pain! (because of the neuropathy that accompanies DM can interfere with neuroreceptors, dulling the pain)

Chest pain – may radiate to the jaw, neck, shoulders, and arm (usually left)

Pain may be accompanied by cool skin, pallor, clammy diaphoresis, tachycardia, and tachypnea

Patients with DM may not experience severe pain! (because of the neuropathy that accompanies DM can interfere with neuroreceptors, dulling the pain)

 

Assessment and Diagnostic Methods Patient History ECG – within 10 minutes of pain onset or arrival at the ER Serial Serum enzymes and isoenzymes (Creatinine Kinase and isoenzymes), myoglobin, and troponin

Patient History

ECG – within 10 minutes of pain onset or arrival at the ER

Serial Serum enzymes and isoenzymes (Creatinine Kinase and isoenzymes), myoglobin, and troponin

WHO criteria have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied: Clinical history of ischaemic type chest pain lasting for more than 20 minutes Changes in serial ECG tracings Rise and fall of serum cardiac enzymes (biomarkers) such as creatine kinase , troponin I, and lactate dehydrogenase isozymes specific for the heart. The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. [25] According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.

WHO criteria have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

Clinical history of ischaemic type chest pain lasting for more than 20 minutes

Changes in serial ECG tracings

Rise and fall of serum cardiac enzymes (biomarkers) such as creatine kinase , troponin I, and lactate dehydrogenase isozymes specific for the heart.

The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. [25] According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.

Right Coronary Artery (RCA) I, aVL II, III, aVF, V 1 , V 4 R, V 5 R, V 6 R Right ventricular (Usually associated with Inferior) Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX) ) V 1 ,V 2 ,V 3 , V 4 V 7 , V 8 , V 9 Posterior (Usually associated with Inferior or Lateral but can be isolated) Circumflex (LCX) or Obtuse Marginal II, III, aVF I, aVL, V 5 , V 6 Lateral Right Coronary Artery (RCA) or Circumflex (LCX) I, aVL II, III, aVF Inferior Left main coronary artery (LCA) II, III, aVF V 1 ,V 2 ,V 3 , V 4 , V 5 , V 6 , I, aVL Extensive anterior (Sometimes called Anteroseptal with Lateral extension) Left Anterior Descending (LAD) , Circumflex (LCX) , or Obtuse Marginal II, III, aVF V 3 , V 4 , V 5 , V 6 , I, aVL Anterolateral Left Anterior Descending (LAD) None V 1 , V 2 , V 3 , V 4 Anteroseptal Left Anterior Descending (LAD) None V 3 , V 4 Anterior Left Anterior Descending (LAD) None V 1 , V 2 Septal Suspected Culprit Artery Leads Showing Reciprocal ST Segment Depression Leads Showing ST Segment Elevation Wall Affected

 

 

 

Electrocardiogram The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populatons. However, the standard 12 lead ECG has several limitations. An ECG represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture. It is therefore desirable to obtain serial 12 lead ECGs , particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring. It should also be appreciated that the standard 12 lead ECG does not directly examine the right ventricle , and does a relatively poor job of examining the posterior basal and lateral walls of the left ventricle . In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG . This can be offset or even eliminated by the use of non-standard ECG leads like the right-sided ECG lead V4R and posterior leads V7, V8, and V9. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care

The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populatons.

However, the standard 12 lead ECG has several limitations. An ECG represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture.

It is therefore desirable to obtain serial 12 lead ECGs , particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring. It should also be appreciated that the standard 12 lead ECG does not directly examine the right ventricle , and does a relatively poor job of examining the posterior basal and lateral walls of the left ventricle .

In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG . This can be offset or even eliminated by the use of non-standard ECG leads like the right-sided ECG lead V4R and posterior leads V7, V8, and V9. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care

The 12 lead ECG is used to classify patients into one of three groups: those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI ), those with ST segment depression or T wave inversion (suspicious for ischemia), and those with a so-called non-diagnostic or normal ECG.

The 12 lead ECG is used to classify patients into one of three groups:

those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI ),

those with ST segment depression or T wave inversion (suspicious for ischemia), and

those with a so-called non-diagnostic or normal ECG.

Right Coronary Artery (RCA) I, aVL II, III, aVF, V 1 , V 4 R, V 5 R, V 6 R Right ventricular (Usually associated with Inferior) Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX) ) V 1 ,V 2 ,V 3 , V 4 V 7 , V 8 , V 9 Posterior (Usually associated with Inferior or Lateral but can be isolated) Circumflex (LCX) or Obtuse Marginal II, III, aVF I, aVL, V 5 , V 6 Lateral Right Coronary Artery (RCA) or Circumflex (LCX) I, aVL II, III, aVF Inferior Left main coronary artery (LCA) II, III, aVF V 1 ,V 2 ,V 3 , V 4 , V 5 , V 6 , I, aVL Extensive anterior (Sometimes called Anteroseptal with Lateral extension) Left Anterior Descending (LAD) , Circumflex (LCX) , or Obtuse Marginal II, III, aVF V 3 , V 4 , V 5 , V 6 , I, aVL Anterolateral Left Anterior Descending (LAD) None V 1 , V 2 , V 3 , V 4 Anteroseptal Left Anterior Descending (LAD) None V 3 , V 4 Anterior Left Anterior Descending (LAD) None V 1 , V 2 Septal Suspected Culprit Artery Leads Showing Reciprocal ST Segment Depression Leads Showing ST Segment Elevation Wall Affected

Management MEDICAL MANAGEMENT: Goal – to minimize myocardial damage, preserve myocardial function, and prevent complications (lethal dysrythmias and cardiogenic shock) Oxygen administration Emergency PTCA Coronary artery bypass or minimally invasive direct coronary artery bypass (MIDCAB) PHARMACOLOGIC THERAPY: Nitrates (nitroglycerine) Anticoagulants (heparin) Analgesics (Morphine) ACE inhibitors Beta blockers Thrombolytics

MEDICAL MANAGEMENT:

Goal – to minimize myocardial damage, preserve myocardial function, and prevent complications (lethal dysrythmias and cardiogenic shock)

Oxygen administration

Emergency PTCA

Coronary artery bypass or minimally invasive direct coronary artery bypass (MIDCAB)

PHARMACOLOGIC THERAPY:

Nitrates (nitroglycerine)

Anticoagulants (heparin)

Analgesics (Morphine)

ACE inhibitors

Beta blockers

Thrombolytics

Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct. Congestive heart failure A myocardial infarction may compromise the function of the heart as a pump for the circulation , a state called heart failure . There are different types of heart failure; left- or right-sided (or bilateral) heart failure may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided MI. Myocardial rupture Myocardial rupture is most common three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later, in as many as 10% of all MIs.[ citation needed ] This may occur in the free walls of the ventricles, the septum between them, the papillary muscles , or less commonly the atria . Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular aneurysm , a localized dilation or ballooning of the heart chamber. Risk factors for myocardial rupture include completion of infarction (no revascularization performed), female sex, advanced age, and a lack of a previous history of myocardial infarction.[ citation needed ] The shear stress between the infarcted segment and the surrounding normal myocardium (which may be hypercontractile in the post-infarction period) makes it a nidus for rupture.[ citation needed ] Rupture is usually a catastrophic event that may result a life-threatening process known as cardiac tamponade , in which blood accumulates within the pericardium or heart sac, and compresses the heart to the point where it cannot pump effectively. Rupture of the intraventricular septum (the muscle separating the left and right ventricles) causes a ventricular septal defect with shunting of blood through the defect from the left side of the heart to the right side of the heart. Rupture of the papillary muscle may also lead to acute mitral regurgitation and subsequent pulmonary edema and possibly even cardiogenic shock .

Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.

Congestive heart failure

A myocardial infarction may compromise the function of the heart as a pump for the circulation , a state called heart failure . There are different types of heart failure; left- or right-sided (or bilateral) heart failure may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided MI.

Myocardial rupture

Myocardial rupture is most common three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later, in as many as 10% of all MIs.[ citation needed ] This may occur in the free walls of the ventricles, the septum between them, the papillary muscles , or less commonly the atria . Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular aneurysm , a localized dilation or ballooning of the heart chamber.

Risk factors for myocardial rupture include completion of infarction (no revascularization performed), female sex, advanced age, and a lack of a previous history of myocardial infarction.[ citation needed ] The shear stress between the infarcted segment and the surrounding normal myocardium (which may be hypercontractile in the post-infarction period) makes it a nidus for rupture.[ citation needed ]

Rupture is usually a catastrophic event that may result a life-threatening process known as cardiac tamponade , in which blood accumulates within the pericardium or heart sac, and compresses the heart to the point where it cannot pump effectively. Rupture of the intraventricular septum (the muscle separating the left and right ventricles) causes a ventricular septal defect with shunting of blood through the defect from the left side of the heart to the right side of the heart. Rupture of the papillary muscle may also lead to acute mitral regurgitation and subsequent pulmonary edema and possibly even cardiogenic shock .

Life-threatening arrhythmia A 12 lead electrocardiogram showing ventricular tachycardia. Since the electrical characteristics of the infarcted tissue change (see pathophysiology section ), arrhythmias are a frequent complication. The re-entry phenomenon may cause too fast heart rates ( ventricular tachycardia and even ventricular fibrillation ), and ischemia in the electrical conduction system of the heart may cause a complete heart block (when the impulse from the sinoatrial node , the normal cardiac pacemaker, doesn't reach the heart chambers any more). Pericarditis As a reaction to the damage of the heart muscle, inflammatory cells are attracted. The inflammation may reach out and affect the heart sac. This is called pericarditis . In Dressler's syndrome , this occurs several weeks after the initial event. Cardiogenic shock A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following it is cardiogenic shock . Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amout of oxygenated blood to the tissues of the body. While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. [86] If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated. [86]

Life-threatening arrhythmia

A 12 lead electrocardiogram showing ventricular tachycardia.

Since the electrical characteristics of the infarcted tissue change (see pathophysiology section ), arrhythmias are a frequent complication. The re-entry phenomenon may cause too fast heart rates ( ventricular tachycardia and even ventricular fibrillation ), and ischemia in the electrical conduction system of the heart may cause a complete heart block (when the impulse from the sinoatrial node , the normal cardiac pacemaker, doesn't reach the heart chambers any more).

Pericarditis

As a reaction to the damage of the heart muscle, inflammatory cells are attracted. The inflammation may reach out and affect the heart sac. This is called pericarditis . In Dressler's syndrome , this occurs several weeks after the initial event.

Cardiogenic shock

A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following it is cardiogenic shock . Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amout of oxygenated blood to the tissues of the body.

While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. [86] If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated. [86]

Valvular heart disease Valvular heart disease is any disease process involving one or more valves of the heart . The valves in the right side of the heart are the tricuspid valve and the pulmonic valve . The valves in the left side of the heart are the mitral valve and the aortic valve .

Valvular heart disease is any disease process involving one or more valves of the heart .

The valves in the right side of the heart are the tricuspid valve and the pulmonic valve .

The valves in the left side of the heart are the mitral valve and the aortic valve .

Each valve may be too narrow ( stenosis ) or too wide or loose, causing regurgitation . There are different types of valvular heart disease: Aortic insufficiency Aortic valve stenosis Endocarditis Heart valve dysplasia Libman-Sacks endocarditis Loeffler endocarditis Mitral regurgitation Mitral stenosis Mitral valve prolapse Pulmonary valve stenosis Tricuspid insufficiency Tricuspid valve stenosis

Each valve may be too narrow ( stenosis ) or too wide or loose, causing regurgitation . There are different types of valvular heart disease:

Aortic insufficiency

Aortic valve stenosis

Endocarditis

Heart valve dysplasia

Libman-Sacks endocarditis

Loeffler endocarditis

Mitral regurgitation

Mitral stenosis

Mitral valve prolapse

Pulmonary valve stenosis

Tricuspid insufficiency

Tricuspid valve stenosis

The Heart with TETRALOGY OF FALLOT In Tetralogy of Fallot , there are four specific defects in the heart: Pulmonary valve stenosis is a narrowing of the pulmonary valve and the area below the valve. This narrowing slows the flow of blood from the right side of the heart to the lungs. The heart must pump harder to push blood through the smaller opening to the lungs where the blood picks up oxygen. Ventricular septal defect (VSD) is a hole in the wall that separates the lower chambers (ventricles) of the heart. Overriding aorta is a defect in the position of the large artery (aorta) that takes oxygen-rich blood to the body. In a normal heart, the aorta attaches to the left lower chamber of the heart (ventricle). In tetralogy of Fallot, the aorta sits between the left and right ventricles, over the VSD. This causes mixing of oxygen-rich blood and oxygen-poor blood. Right ventricular hypertrophy is the thickening of the right lower chamber of the heart (ventricle). Unlike other muscles in your body, when the heart thickens, it does not work well. The heart has to pump harder to move blood through the narrowed pulmonary valve and the area below it.

In Tetralogy of Fallot , there are four specific defects in the heart:

Pulmonary valve stenosis is a narrowing of the pulmonary valve and the area below the valve. This narrowing slows the flow of blood from the right side of the heart to the lungs. The heart must pump harder to push blood through the smaller opening to the lungs where the blood picks up oxygen.

Ventricular septal defect (VSD) is a hole in the wall that separates the lower chambers (ventricles) of the heart.

Overriding aorta is a defect in the position of the large artery (aorta) that takes oxygen-rich blood to the body. In a normal heart, the aorta attaches to the left lower chamber of the heart (ventricle). In tetralogy of Fallot, the aorta sits between the left and right ventricles, over the VSD. This causes mixing of oxygen-rich blood and oxygen-poor blood.

Right ventricular hypertrophy is the thickening of the right lower chamber of the heart (ventricle). Unlike other muscles in your body, when the heart thickens, it does not work well. The heart has to pump harder to move blood through the narrowed pulmonary valve and the area below it.

The Heart with TETRALOGY OF FALLOT Pulmonary Valve stenosis; 2. VSD; 3. Overriding of the Aorta; 4.RVH

Pulmonary Valve stenosis; 2. VSD; 3. Overriding of the Aorta; 4.RVH

These defects can cause: Less blood flow to the lungs. Mixing of oxygen-rich (red) and oxygen-poor (blue) blood inside the heart. Low levels of oxygen in the blood. When oxygen levels are low, the baby's skin, fingertips, or lips have a bluish tint. This condition is called cyanosis (SY-uh-NO-sis). An infant with cyanosis is sometimes called a "blue baby." Each year in the United States, about 3,000 babies are born with tetralogy of Fallot. It is the congenital heart defect that causes the most cases of cyanosis. Every infant or child with tetralogy of Fallot needs surgery, usually within the first year of life. Because of advances in surgery and treatment, many children born with tetralogy of Fallot have successful surgery and live to adulthood.

These defects can cause:

Less blood flow to the lungs.

Mixing of oxygen-rich (red) and oxygen-poor (blue) blood inside the heart.

Low levels of oxygen in the blood.

When oxygen levels are low, the baby's skin, fingertips, or lips have a bluish tint. This condition is called cyanosis (SY-uh-NO-sis). An infant with cyanosis is sometimes called a "blue baby."

Each year in the United States, about 3,000 babies are born with tetralogy of Fallot. It is the congenital heart defect that causes the most cases of cyanosis.

Every infant or child with tetralogy of Fallot needs surgery, usually within the first year of life. Because of advances in surgery and treatment, many children born with tetralogy of Fallot have successful surgery and live to adulthood.

CARDIAC CONDUCTION SYSTEM

In the normal human heart each heart beat originates in the Sinoatrial node (SA node) , which is the heart's normal pacemaker. The SA node is located in the upper- posterior wall of the right atrium and initiates a depolarization wave at regular intervals to bring about contraction of the heart. Normally, the SA node generates an electrical impulse which travels through the right and left atrial muscles producing electrical changes which is represented on the electrocardiogram (ECG) by the P-wave . The electrical impulse then travels through the atrioventricular node (AV Node), which conducts electricity at a slower speed. This will create a pause ( PR interval ) before the ventricles are stimulated. This pause is helpful since it allows blood to be emptied into the ventricles from the atria prior to ventricular contraction to push blood out into the body. The QRS complex (in the ECG) represents ventricular contraction. This is followed by the T-wave which corresponds to the electrical changes in the ventricles as they relax and the whole process is repeated.

In the normal human heart each heart beat originates in the Sinoatrial node (SA node) , which is the heart's normal pacemaker.

The SA node is located in the upper- posterior wall of the right atrium and initiates a depolarization wave at regular intervals to bring about contraction of the heart.

Normally, the SA node generates an electrical impulse which travels through the right and left atrial muscles producing electrical changes which is represented on the electrocardiogram (ECG) by the P-wave .

The electrical impulse then travels through the atrioventricular node (AV Node), which conducts electricity at a slower speed.

This will create a pause ( PR interval ) before the ventricles are stimulated. This pause is helpful since it allows blood to be emptied into the ventricles from the atria prior to ventricular contraction to push blood out into the body.

The QRS complex (in the ECG) represents ventricular contraction.

This is followed by the T-wave which corresponds to the electrical changes in the ventricles as they relax and the whole process is repeated.

The discharge rate of the SA node determines the heart rate, which is the number of times the heart beats per minute. At rest, the heart beats about 70 times a minute. However, the sinus rhythm maintains a rate of 60-100 beats per minute, which is the normal range of the pacing rate. A rhythm originating in the heart's SA node with a rate slower than 50 beats per minute is called Sinus Bradycardia . Sinus tachycardia occurs when the sinus rhythm is faster than 100 beats per minute and results from increased automaticity of the SA node. The heart rate is slowed during sleep and accelerated by emotion, exercise, fever and other stimuli.

The discharge rate of the SA node determines the heart rate, which is the number of times the heart beats per minute.

At rest, the heart beats about 70 times a minute. However, the sinus rhythm maintains a rate of 60-100 beats per minute, which is the normal range of the pacing rate.

A rhythm originating in the heart's SA node with a rate slower than 50 beats per minute is called Sinus Bradycardia .

Sinus tachycardia occurs when the sinus rhythm is faster than 100 beats per minute and results from increased automaticity of the SA node.

The heart rate is slowed during sleep and accelerated by emotion, exercise, fever and other stimuli.

Approximate normal conduction velocity at each part of the pathway is summarized below: 0.5 m/s Ventricular Tissue 1-4 m/s Purkinje Fibers 2 m/s Bundle Branches 2 m/s His Bundle 0.05 m/s AV Node 1 m/s Atrial Tissue Conduction velocity Location

 

 

ANEURYSM, AORTIC Aneurysm is a localized sac or dilatation of an artery formed at a weak point in the vessel wall Most common cause: Atherosclerosis Other causes: arterial wall trauma, infection (pyogenic, or syphilitic), and congenital defects of the arterial wall Most common forms: Saccular anerysm – one side of the vessel only Fusiform aneurysm– involve dilatation of the entire arterial segment Mycotic aneurysm – small anerysm due to local infections Aortic aneurysm Thorasic Abdominal Dissecting Men are affected more than women Rupture can lead to hemorrhage and death

Aneurysm is a localized sac or dilatation of an artery formed at a weak point in the vessel wall

Most common cause:

Atherosclerosis

Other causes: arterial wall trauma, infection (pyogenic, or syphilitic), and congenital defects of the arterial wall

Most common forms:

Saccular anerysm – one side of the vessel only

Fusiform aneurysm– involve dilatation of the entire arterial segment

Mycotic aneurysm – small anerysm due to local infections

Aortic aneurysm

Thorasic

Abdominal

Dissecting

Men are affected more than women

Rupture can lead to hemorrhage and death

THORASIC AORCTIC ANEURYSM Occur most frequent in men between ages 40 and 70 years Thoracic area is the most common site for dissecting aneurysm About one-third of patients die from rupture ABDOMINAL ANEURYSM Most common among whites between ages 60 and 90 years Most common below the renal arteries 40% have symptoms Risk factors: genetic predisposition, smoking, hypertension DISSECTING ANEURYSM Caused by rupture in the intimal layer, by blood dissecting the vessel layers Associated with poorly controlled hypertension 3x more common in men between ages 50 and 70 years

THORASIC AORCTIC ANEURYSM

Occur most frequent in men between ages 40 and 70 years

Thoracic area is the most common site for dissecting aneurysm

About one-third of patients die from rupture

ABDOMINAL ANEURYSM

Most common among whites between ages 60 and 90 years

Most common below the renal arteries

40% have symptoms

Risk factors: genetic predisposition, smoking, hypertension

DISSECTING ANEURYSM

Caused by rupture in the intimal layer, by blood dissecting the vessel layers

Associated with poorly controlled hypertension

3x more common in men between ages 50 and 70 years

Clinical Manifestations Variable symptoms Depend on how rapid the aneurysm dilates Affects the sorrounding intrathoracic structures Thoracic aortic aneurysm: boring pain; dyspnea, cough, or stridor; hoarseness, weak voice, aphonia; dysphagia; dilated superficial veins on chest, neck, or arms; edematous areas on chest wall; cyanosis; unequal pupils Abdominal aortic aneurysm: “heart beating”; “blue-toe syndrome” (occlusion of digital vessels); severe back or abdominal pain (sign of impending rupture) Dissecting aneurysm: sudden onset of severe, persistent “tearing” or “ripping” pain over the interior chect or back, extending to the shoulders, epigastric area, or abdomen; pallor, sweating, and tachycardia; elevated BP or markedly different from one arm to the other; and death usually caused by external rupture of the hematoma

Variable symptoms

Depend on how rapid the aneurysm dilates

Affects the sorrounding intrathoracic structures

Thoracic aortic aneurysm: boring pain; dyspnea, cough, or stridor; hoarseness, weak voice, aphonia; dysphagia; dilated superficial veins on chest, neck, or arms; edematous areas on chest wall; cyanosis; unequal pupils

Abdominal aortic aneurysm: “heart beating”; “blue-toe syndrome” (occlusion of digital vessels); severe back or abdominal pain (sign of impending rupture)

Dissecting aneurysm: sudden onset of severe, persistent “tearing” or “ripping” pain over the interior chect or back, extending to the shoulders, epigastric area, or abdomen; pallor, sweating, and tachycardia; elevated BP or markedly different from one arm to the other; and death usually caused by external rupture of the hematoma

Assessment and Diagnostic Methods Chest radiograph Angiogram Transesophageal echocardiography MRI Ultasonography or CT scan – determine size, length, location of aneurysm Systolic bruit – heard on auscultation over the pulsating mass of the abdominal aortic aneurysm at the middle and upper abdomen

Chest radiograph

Angiogram

Transesophageal echocardiography

MRI

Ultasonography or CT scan – determine size, length, location of aneurysm

Systolic bruit – heard on auscultation over the pulsating mass of the abdominal aortic aneurysm at the middle and upper abdomen

Management – Medical / Surgical Medical or Surgical treatment depends on the type of aneurysm Poor prognosis for ruptured aneurysm and surgery is performed immediately Medical Measures: Strict control of BP and reduction in pulsatile flow Systolic pressure maintained at 100 to 120 mmHg (i.e. Nitroprusside ) Pulsatile flow reduction with reduce cardiac contractility (i.e. Propranolol ) Surgical Management: Goal: Removal of the aneurysm and restoration of vascular continuity with graft (resection and bypass graft or endovascular grafting – the treatment of choice for abdominal aortic aneurysm larger than 5cm (2 inches) in diameter or enlarging Intensive monitoring in the Critical Care Unit is required

Medical or Surgical treatment depends on the type of aneurysm

Poor prognosis for ruptured aneurysm and surgery is performed immediately

Medical Measures:

Strict control of BP and reduction in pulsatile flow

Systolic pressure maintained at 100 to 120 mmHg (i.e. Nitroprusside )

Pulsatile flow reduction with reduce cardiac contractility (i.e. Propranolol )

Surgical Management:

Goal: Removal of the aneurysm and restoration of vascular continuity with graft (resection and bypass graft or endovascular grafting – the treatment of choice for abdominal aortic aneurysm larger than 5cm (2 inches) in diameter or enlarging

Intensive monitoring in the Critical Care Unit is required

ANEURYSM, INTRACRANIAL Intracranial (cerebral) aneurysm – dilatation of the walls of the cerebral artery as a result of weakness in the arterial wall Causes: Unknown Maybe due to atherosclerosis, congenital defects of the arterial walls, hypertensive vascular disease, head trauma, or advancing age Commonly affects the internal carotid, anterior or posterior cerebral, anterior or posterior communicating, and middle cerebral arteries Symptoms are produced when the aneurysm enlarges and presses on the nearby cranial nerves or brain tissue, or ruptures, causing Subarachnoid hemorrhage. Prognosis depends on the age and neurologic condition of patient, associated diseases, and extent and location of the aneurysm

Intracranial (cerebral) aneurysm – dilatation of the walls of the cerebral artery as a result of weakness in the arterial wall

Causes:

Unknown

Maybe due to atherosclerosis, congenital defects of the arterial walls, hypertensive vascular disease, head trauma, or advancing age

Commonly affects the internal carotid, anterior or posterior cerebral, anterior or posterior communicating, and middle cerebral arteries

Symptoms are produced when the aneurysm enlarges and presses on the nearby cranial nerves or brain tissue, or ruptures, causing Subarachnoid hemorrhage.

Prognosis depends on the age and neurologic condition of patient, associated diseases, and extent and location of the aneurysm

Clinical Manifestations With rupture: Sudden unusually severe headache Loss of consciousness Pain and rigidity of the back of the neck and spine Visual disturbances (visual loss, diplopia, ptosis) Tinnitus, dizziness, and hemiparesis If the aneurysm leaks and forms clot: Show little neurologic deficit, or severe bleeding , resulting in cerebral damage followed rapidly by coma and death.

With rupture:

Sudden unusually severe headache

Loss of consciousness

Pain and rigidity of the back of the neck and spine

Visual disturbances (visual loss, diplopia, ptosis)

Tinnitus, dizziness, and hemiparesis

If the aneurysm leaks and forms clot:

Show little neurologic deficit, or severe bleeding , resulting in cerebral damage followed rapidly by coma and death.

Assessment and Diagnostic Methods CT scan Cerebral angiography Lumbar puncture Hunt – Hess Classification of Clinical Grades – guide for diagnosing the severity of Subarachnoid hemorrhage after an aneurysm bleeds

CT scan

Cerebral angiography

Lumbar puncture

Hunt – Hess Classification of Clinical Grades – guide for diagnosing the severity of Subarachnoid hemorrhage after an aneurysm bleeds

Medical Management Allow the brain to recover from the initial bleeding Prevent or minimize the risk of rebleeding Prevent or treat other complications : rebleeding, cerebral vasospasm, acute hydrocephalus, and seizures Provide bed rest with sedation to prevent agitation and stress Maintain cerebral blood flow and oxygenation ; maintain hemoglobin and hematocrit levels and adequate hydration. Avoid blood presure extremes (Hypertension or Hypotension) Manage vasospasm with calcium-channel blockers (i.e. Nimodipine, Verapamil, and Nifedipine ). Endovascular technique may also be used Arterial bypass or medical treatment to prevent rebleeding Manage increased intracranial pressure (ICP) by draining cerebrospinal fluid (CSF) via LP or ventricular catheter drainage Administer Mannitol to reduce ICP, and monitor for signs of dehydration and rebound elevation of ICP Administer fibrinolytic agents to delay or prevent dissolution of the clot if surgery is delayed or contraindicated

Allow the brain to recover from the initial bleeding

Prevent or minimize the risk of rebleeding

Prevent or treat other complications : rebleeding, cerebral vasospasm, acute hydrocephalus, and seizures

Provide bed rest with sedation to prevent agitation and stress

Maintain cerebral blood flow and oxygenation ; maintain hemoglobin and hematocrit levels and adequate hydration. Avoid blood presure extremes (Hypertension or Hypotension)

Manage vasospasm with calcium-channel blockers (i.e. Nimodipine, Verapamil, and Nifedipine ). Endovascular technique may also be used

Arterial bypass or medical treatment to prevent rebleeding

Manage increased intracranial pressure (ICP) by draining cerebrospinal fluid (CSF) via LP or ventricular catheter drainage

Administer Mannitol to reduce ICP, and monitor for signs of dehydration and rebound elevation of ICP

Administer fibrinolytic agents to delay or prevent dissolution of the clot if surgery is delayed or contraindicated

 

 

Stroke is the third leading cause of death in America and the No. 1 cause of adult disability. 80% of strokes are preventable YOU CAN PREVENT STROKE ! Cerebro-Vascular Accident

Stroke is the third leading cause of death in America and the No. 1 cause of adult disability.

80% of strokes are preventable

YOU CAN PREVENT STROKE !

What is Stroke ? A stroke or "brain attack" occurs when a blood clot blocks an artery (a blood vessel that carries blood from the heart to the body) or a blood vessel (a tube through which the blood moves through the body) breaks, interrupting blood flow to an area of the brain.  When either of these things happen, brain cells begin to die and brain damage occurs.

A stroke or "brain attack" occurs when a blood clot blocks an artery (a blood vessel that carries blood from the heart to the body) or a blood vessel (a tube through which the blood moves through the body) breaks, interrupting blood flow to an area of the brain. 

When either of these things happen, brain cells begin to die and brain damage occurs.

When brain cells die during a stroke, abilities controlled by that area of the brain are lost. These abilities include speech, movement and memory. How a stroke patient is affected depends on where the stroke occurs in the brain and how much the brain is damaged. For example, someone who has a small stroke may experience only minor problems such as weakness of an arm or leg. People who have larger strokes may be paralyzed on one side or lose their ability to speak. Some people recover completely from strokes, but more than 2/3 of survivors will have some type of disability.

When brain cells die during a stroke, abilities controlled by that area of the brain are lost.

These abilities include speech, movement and memory.

How a stroke patient is affected depends on where the stroke occurs in the brain and how much the brain is damaged.

For example, someone who has a small stroke may experience only minor problems such as weakness of an arm or leg.

People who have larger strokes may be paralyzed on one side or lose their ability to speak.

Some people recover completely from strokes, but more than 2/3 of survivors will have some type of disability.

Stroke as the primary neurologic problem in the US and in the world 15% Hemorrhagic 85% Ischemic/Nonhemorrhagic Stroke categories according to cause: Thrombosis 20% Small penetrating thrombosis 25% Cardiogenic embolic stroke, cryptogenic (unknown cause) 25% Others ( cocaine use, coagulopathies, migraine, spontaneous dissection of the carotid or vetebral arteries 5% Stroke classified according to the time course: Transient ischemic attack (TIA) Reversible ischemic neurologic deficit (RIND) Stroke in evolution Completed stroke

Stroke as the primary neurologic problem in the US and in the world

15% Hemorrhagic

85% Ischemic/Nonhemorrhagic

Stroke categories according to cause:

Thrombosis 20%

Small penetrating thrombosis 25%

Cardiogenic embolic stroke, cryptogenic (unknown cause) 25%

Others ( cocaine use, coagulopathies, migraine, spontaneous dissection of the carotid or vetebral arteries 5%

Stroke classified according to the time course:

Transient ischemic attack (TIA)

Reversible ischemic neurologic deficit (RIND)

Stroke in evolution

Completed stroke

Risk Factors Hemorrhragic strokes: arteriovenous malformations (AVM’s), aneurysm ruptures, certain drugs, uncontrolled hypertension, hemangioblastomas, and trauma Ischemic strokes: cardiovascular disease (cerebral embolism may originate in the heart) and dysrhythmia (atrial fibrillation); risk factors for CAD; vasospasm, migraines, and coagulopathies (high hematocrit) General cerebral ischemia maybe caused by excessive or prolonged drop in BP Drug abuse (cocaine), particularly in adolescents and young adults Alcohol consumption may also be a risk factor

Hemorrhragic strokes: arteriovenous malformations (AVM’s), aneurysm ruptures, certain drugs, uncontrolled hypertension, hemangioblastomas, and trauma

Ischemic strokes: cardiovascular disease (cerebral embolism may originate in the heart) and dysrhythmia (atrial fibrillation); risk factors for CAD; vasospasm, migraines, and coagulopathies (high hematocrit)

General cerebral ischemia maybe caused by excessive or prolonged drop in BP

Drug abuse (cocaine), particularly in adolescents and young adults

Alcohol consumption may also be a risk factor

Clinical Manifestations General signs and symptoms: Numbness or weakness of the face, arm, or leg Confusion or change in mental status Trouble speaking or understanding speech Visual disturbances Loss of balance Dizziness Difficulty in walking Sudden severe headache

General signs and symptoms:

Numbness or weakness of the face, arm, or leg

Confusion or change in mental status

Trouble speaking or understanding speech

Visual disturbances

Loss of balance

Dizziness

Difficulty in walking

Sudden severe headache

MOTOR LOSS Hemiplegia, hemiparesis Flaccid paralysis and loss of or decrease in deep tendon reflexes (initial) and increased muscle tone (spasticity after 48 hrs) COMMUNICATION LOSS Dysarthria (difficulty in speaking) Dysphasia or aphasia (defective or loss of speech) Apraxia (inability to perform a prviously learned action) PERCEPTUAL DISTURBANCES AND SENSORY LOSS Visual perceptual dysfunctions (homonymous hemianopia – loss half of the visual field) Disturbances in visuospatial relationship – left hemispheric damage Sensory losses: impair touch or severe loss of propioception, difficulty in interrupting visual, tactile, and auditory stimuli IMPAIRED CIGNITIVE AND PSYCHOLOGICAL EFFECTS Impaired learning capacity, memory, or other higher cortical intellectual functions common in frontal lobe damage – limited attention span, difficulties in comprehension, forgetfullness, and lack of motivation Depression, other psychological problems: emotional lability, hostility, frustration, resentment, and lack of cooperation BLADDER DYSFUNCTION Transient urinary incontinence Persistent urinary incontinence or urinary retention Continuing bladder and bowel incontinence

MOTOR LOSS

Hemiplegia, hemiparesis

Flaccid paralysis and loss of or decrease in deep tendon reflexes (initial) and increased muscle tone (spasticity after 48 hrs)

COMMUNICATION LOSS

Dysarthria (difficulty in speaking)

Dysphasia or aphasia (defective or loss of speech)

Apraxia (inability to perform a prviously learned action)

PERCEPTUAL DISTURBANCES AND SENSORY LOSS

Visual perceptual dysfunctions (homonymous hemianopia – loss half of the visual field)

Disturbances in visuospatial relationship – left hemispheric damage

Sensory losses: impair touch or severe loss of propioception, difficulty in interrupting visual, tactile, and auditory stimuli

IMPAIRED CIGNITIVE AND PSYCHOLOGICAL EFFECTS

Impaired learning capacity, memory, or other higher cortical intellectual functions common in frontal lobe damage – limited attention span, difficulties in comprehension, forgetfullness, and lack of motivation

Depression, other psychological problems: emotional lability, hostility, frustration, resentment, and lack of cooperation

BLADDER DYSFUNCTION

Transient urinary incontinence

Persistent urinary incontinence or urinary retention

Continuing bladder and bowel incontinence

Assessment and Diagnostic Methods Complete Physical and Neurologic Examination Non-contrast CT or MRI scan Transthoracic or transesophageal echocardiogram Carotid ultrasonography Cerebral angiography Transcranial Doppler flow studies Electrocardiography Prevention Help patient alter risk factors for stroke Prepare and support patient through carotid endarterectomy Administer anticoagulant agents as ordered

Complete Physical and Neurologic Examination

Non-contrast CT or MRI scan

Transthoracic or transesophageal echocardiogram

Carotid ultrasonography

Cerebral angiography

Transcranial Doppler flow studies

Electrocardiography

Prevention

Help patient alter risk factors for stroke

Prepare and support patient through carotid endarterectomy

Administer anticoagulant agents as ordered

Medical Management Recombinant tissue plasminogen activator (t-pA), unless contraindicated; monitor for bleeding Management of increased ICP: osmotic diuretics, maintain PaCO 2 at 30 – 35 mmHg, avoid hypoxia, elevate head of bed, pulmonary toilet with supllemental oxygen, airway patency Intubation with an ET to establish patent airway, if necessary Maintain cardiac output at 4 – 8 L/min Anticoagulation therapy Carotid endarterectomy (for managing TIA, and small stroke) Management of Complications Cerebral hypoxia: administer supplemental oxygen, maintain hemoglobin and hematocrit at acceptable levels Decreased cerebral blood flow and extension of the area of injury: adequate hydration, avoid hypertension or hypotension

Recombinant tissue plasminogen activator (t-pA), unless contraindicated; monitor for bleeding

Management of increased ICP: osmotic diuretics, maintain PaCO 2 at 30 – 35 mmHg, avoid hypoxia, elevate head of bed, pulmonary toilet with supllemental oxygen, airway patency

Intubation with an ET to establish patent airway, if necessary

Maintain cardiac output at 4 – 8 L/min

Anticoagulation therapy

Carotid endarterectomy (for managing TIA, and small stroke)

Management of Complications

Cerebral hypoxia: administer supplemental oxygen, maintain hemoglobin and hematocrit at acceptable levels

Decreased cerebral blood flow and extension of the area of injury: adequate hydration, avoid hypertension or hypotension

MYASTHENIA GRAVIS An autoimmune disorder affecting the myoneural junction Antibodies or autobodies are directed at the neurotransmitter (acetylcholine) receptor on the motor end plate – disrupt the transmission of transmission of voluntary muscles of the body Excessive weakness and fatigability occurs Affects women between ages 20 and 40 years Affects men older than 40 years

An autoimmune disorder affecting the myoneural junction

Antibodies or autobodies are directed at the neurotransmitter (acetylcholine) receptor on the motor end plate – disrupt the transmission of transmission of voluntary muscles of the body

Excessive weakness and fatigability occurs

Affects women between ages 20 and 40 years

Affects men older than 40 years

Clinical Manifestations Purely a motor disorder, with no effect on sensation or coordination, extreme muscular weakness and easy fatigability, which worsen after effort and are relieved by rest Symptoms vary according to the muscles affected: early symptoms: diplopia and ptosis Sleepy masklike expression because facial muscles are affected Dysphonia (voice inpairment), with nasal sound or difficulty in articulation Problems with chewing and swallowing, which can present danger of choking and aspiration Weakness of arm and hand muscles, less commonly leg muscles Progressive weakness of diaphragm and intercoastal muscles, which may produce respiratory distress (acute emergency)

Purely a motor disorder, with no effect on sensation or coordination, extreme muscular weakness and easy fatigability, which worsen after effort and are relieved by rest

Symptoms vary according to the muscles affected:

early symptoms: diplopia and ptosis

Sleepy masklike expression because facial muscles are affected

Dysphonia (voice inpairment), with nasal sound or difficulty in articulation

Problems with chewing and swallowing, which can present danger of choking and aspiration

Weakness of arm and hand muscles, less commonly leg muscles

Progressive weakness of diaphragm and intercoastal muscles, which may produce respiratory distress (acute emergency)

Assessment and Diagnostic Evaluation Presumptive diagnosis based on history and PE – patient presents with ocular, bulbar symptoms or fluctuating weakness will need a diagnostic workup for MG Injection of Endrophonium (Tensilon) – confirms the diagnosis (improve muscle strength represent a positive test) MRI – enlarged thymus gland Serum analysis for acetylcholine receptor and EMG to measure electrical potential of muscle cells

Presumptive diagnosis based on history and PE – patient presents with ocular, bulbar symptoms or fluctuating weakness will need a diagnostic workup for MG

Injection of Endrophonium (Tensilon) – confirms the diagnosis (improve muscle strength represent a positive test)

MRI – enlarged thymus gland

Serum analysis for acetylcholine receptor and EMG to measure electrical potential of muscle cells

Complications Myasthenia Crisis Result of under medication or no cholinergic medication Result from progression of the disease, emotional upset, systemic infections, medications, surgery, or trauma Manifested as sudden onset of acute respiratory distress and inability to swallow or speak Cholinergic Crisis Caused by overmedication with cholinergic or anti-cholinesterase drugs Produce muscle weakness and the respiratory depression of myasthenia crisis and gastrointestinal symptoms (nausea, vomiting

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