ACUTE BIOLOGICAL CRISIS

these are conditions that may result to patient mortality if left unattended in a brief period of time. These are conditions that warrants immediate attention for the reversal of disease process & prevention of further morbidity & mortality.

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Conditions: 1. Cardiac failure & dysrhythmias 2. Respiratory failures & ARDS 3. Renal Failure & ESRD 4. Burns 5. Hepatic coma 6. Diabetic ketoacidosis 7. Thyroid crisis & adrenal crisis 8. Multisystem organ failure & shock

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ACUTE BIOLOGICAL CRISIS

Ms. Jenneth E. dela Cerna, R.N.

3

RENAL FAILURE
4

RENAL FAILURE Results when the kidneys are unable to remove the bodys metabolic wastes or perform their regulatory functions. Substances normally eliminated in the urine accumulate in the body.

ACUTE RENAL FAILURE

is a sudden and almost complete loss of kidney function [decreased GFR] over a period of hours to days. Reversible

1.

Prerenal [hypoprefusion of kidneys] Volume depletion Impaired cardiac performance Vasodilation

6

Categories of Acute Renal Failure:

2.

Intrarenal [actual damage of kidney tissues] Prolonged renal ischemia Nephrotoxic agents Infectious processes
Postrenal [obstruction of urine flow] Calculi Tumors BPH Strictures Blood clots

3.

PHASES OF ACUTE RENAL FAILURE:

1.

INITIATION PERIOD
Begins with the initial insult & ends when oliguria develops.

2.

PERIOD OF OLIGURIA
Accompanied by a rise in serum concentration of substances usually excreted by the kidneys. Appearance of uremic symptoms & hyperkalemia

3.

PERIOD OF DIURESIS
Gradual increase in urine output Laboratory values stop rising Observed closely for dehydration

4.

PERIOD OF RECOVERY
Signals the improvement of the renal function 3-12 months Normal laboratory values Permanent 1-3% of reduction in GFR

Clinical manifestations: Oliguria to anuria Edema Dry mucous membrane Uremic fetor & uremic frost Nausea and vomiting Drowsiness, headache, seizures (azotemia) Ill & lethargy Cardiac dysrhythmias Anemia Hypertension Pruritus

10

Diagnostic Findings: Urine changes hematuria/proteinuria Hyperkalemia Increased BUN & creatinine level Metabolic acidosis Electrolyte imbalance Anemia ECG changes

11

Medical management
Determine the cause Dialysis may be indicated in severe azotemia Fluid balance diuretic can be prescribe if edema is present. Kayexalate/Insulin/Calcium Gluconate Low dose of dopamine Sodium bicarbonate Aluminum hydroxide High carbohydrate, potassium and sodium restricted diet. Low protein during oliguric phase, high protein during recovery phase
12

Nursing management Monitoring Fluid and electrolytes Reducing metabolic rate Promoting pulmonary function Preventing infection Providing skin care

13

CHRONIC RENAL FAILURE

is a progressive, irreversible deterioration in renal function in which the bodys ability to maintain metabolic and fluid and electrolyte balance fails, resulting to uremia or azotemia. kidney sustain irreversible damage. Fatal without treatment
CAUSES: Diabetes mellitus (leading cause) Hypertension Acute Glomerulonephritis Pyelonephritis Obstruction

14

Clinical Manifestations: hypertension edema and pulmonary edema pruritus uremic frost anorexia, nausea and vomiting altered level of consciousness, restlessness seizure creatinine and BUN increase (decreased GFR) metabolic acidosis anemia and bleeding tendencies electrolytes imbalance oliguria to anuria
15

Stages of Chronic Renal failure

1.

Decrease renal reserve [60-89%] asymptomatic homeostasis Renal insufficiency [30-59%] Renal failure [15-29%] ESRD or End Stage Renal Disease [<15%] final stage no homeostasis
16

2.

3.

4.

Complications: 1. Hyperkalemia 2. Pericarditis, pericardial effusion 3. Anemia 4. Bone diseases 5. Hypertension Medical Management: 1. Pharmacologic Therapy Antacids Aluminum based antacids Calcium carbonate Avoid magnesium based antacids Antihypertensive Diuretics Epogen
17

2.

Nutritional Therapy Protein restricted diet Potassium restricted diet Regulate Sodium and fluid intake vitamin supplements Other Therapy: Kayexalate Dialysis Kidney transplant

3.

Nursing management: The same with Acute renal failure

18

HEPATIC ENCEPHALOPATHY COMA

AND

A life-threatening complication of liver disease. results from the accumulation of ammonia and other toxic metabolites in the blood. Hepatic coma represents the most advanced stage of hepatic encephalopathy.

Ammonia accumulation

Enters the bloodstream

Passes to the blood brain barrier

Brain dysfunction and damage

HEPATIC ENCEPHALOPATHY

CLINICAL MANIFESTATIONS:
Earliest symptoms: 1. Minor mental changes and motor disturbances 2. Confused and unkempt 3. Altered sleep patterns, restlessness 4. Fetor hepaticus Fruity, musty breath odor similar to that of freshly mowed grass, acetone or old wine.

5. 6. 7.

Asterixis or liver flap Constructional apraxia With further progression of the disorder, the patient lapses into frank coma and may have seizures.

MEDICAL MANAGEMENT:
1.

Lactulose (Duphalac) To reduce serum ammonia levels. Draws the ammonia from the blood into the colon & removed from the body. Changes fecal flora to organisms that do not produce ammonia from urea. 2-3 stools per day. Nursing alert! The patient receiving lactulose is monitored closely for the development of watery diarrheal stools, because they indicate a medication overdose.

2. 3.

I.V administration of glucose. Neomycin Sulfate

Decreases the normal flora in the intestines to reduce bacterial activity on protein.

NURSING MANAGEMENT
1.

2.
3. 4.

5.
6. 7. 8. 9.

Neurologic status is assessed frequently. A daily record of handwriting specimen is kept. Maintaining a safe environment. Provide small, frequent meals and an evening snacks of complex CHO to avoid CHON overloading. Monitor intake & output. Monitor serum ammonia level as ordered. Protein diet restriction. Limit activity. Prevent GI bleeding. Monitor for side effects of medications.

ADRENAL CORTEX:
Addisons disease Cushings syndrome Aldosteronism (Conns Syndrome)

26

ADDISONS DISEASE

Addison's disease occurs when the adrenal glands do not produce enough of the hormone cortisol and, in some cases, the hormone aldosterone.

Hyposecretion of the adrenal cortex hormones

90% of the gland is destroyed

The disease is also called adrenal insufficiency, or hypocortisolism Either primary or secondary can progress to adrenal crisis.

Adrenal crisis (Addisonian crisis) - Is a deficiency of mineralocorticoid & glucocorticoid that requires immediate treatment

ADDISONIAN CRISIS
Life-threatening disorder caused by acute adrenal insufficiency precipitated by stress, infection, trauma or surgery. Causes: hyponatremia, hypoglycemia, hyperkalemia & shock. Given glucocorticoids IV: e.g. hydrocortisone Na succinate (SoluCortef), mineralocorticoids e.g. fludrocortisone (Florinef) Severe, generalized muscle weakness, severe hypotension, hypovolemia, shock (vascular collapse), irritability & confusion, hypoglycemia, Increased BUN; rapid respiratory rate; rapid weak pulse Check BP & electrolyte levels Strict bed rest in quiet environment & protect from infection.28

CUSHINGS SYNDROME/CUSHINGS DISEASE

Hypersecretion of glucocorticoids from the adrenal cortex. Cushings disease is a metabolic disorder characterized by abnormally increased secretion (endogenous) of cortisol caused by an increased amounts of ACTH secreted by the pituitary gland.

30

Etiology: Adrenal tumor Ectopic ACTH production by malignancies Long steroid usage ASSESSMENT: Subjective: Generalized muscle weakness & wasting Moonface, buffalo hump Truncal obesity with thin extremities, weight gain Hirsutism Hyperglycemia, hypernatremia Hypokalemia Hypertension Pendulous abdomen, purple straiae, easy bruising

31

Diagnosis
24-hour urine cortisol ACTH levels determination

Serum Na, K
FBS/HGT Radiographic studies

Skull series
CT scan/MRI

32

NURSING MANAGEMENT:

Promote comfort: protect from trauma. Prevent complications: monitor fluid balance, glucose metabolism, hypertension, infection. Health teachings: a. Diet: increased protein, potassium, decreased calories, sodium b. Meds: Cytoxic agents: aminoglutethimide (Cytaden), trilostane (Modrastane), mitotane (Lysodren)- to decrease cortisol production. Replacement hormones as needed. c. S/Sx of progression of disease. d. Prepare client for adrenalectomy.
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DIABETIC KETOACIDOSIS
a. b. c.

d.

is an acute complication of hyperglycemic crisis. it is a life threatening complication of DM 1 Causes: Infection/Illness Surgery Stress Insufficient or absent insulin

34

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PATHOPHYSIOLOGY
absence of endogenous insulin
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decreased glucose cellular uptake hyperglycemia body breaks down fats fatty acids ketone bodies diabetic ketoacidosis -------hyperkalemia coma

35

CLINICAL MANIFESTATIONS:
1. 2. 3. 4. 5. 6.

7.
8. 9. 10.

11.
12. 13.

Drowsiness Coma Severe dehydration Fruity breath odor Rapid & deep breathing Polyuria, polyphagia, polydipsia Weight loss Muscle wasting Vision changes Recurrent infections Abdominal cramps Nausea & vomiting Leg cramps

36

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DIAGNOSTIC EVALUATION:
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Serum glucose: 200-800 mg/dl Positive urine acetone Arterial blood gas analysis Serum potassium Electrocardiogram (Tall tented T waves, widened QRS)

flattened T wave & presence of U wave

37

MEDICAL

MANAGEMENT:
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1. Iv adminstration

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CARDIOVASCULAR

DISORDERS

39

Enclosed within the inferior mediastinum. Enclosed by a double sac of serous membrane Pericardium Lubricating fluid that is produced by the serous pericardial membranes. Allows heart to beat easily.

THE HEART

Serous fluid

Pericarditis:

Decreased in the amount of serous fluid adhesions

interfere with the heart movement
40

Wednesday, June 20, 2012

3 LAYERS OF THE HEART WALLS: 1. Epicardium tightly hugs the external surface of the heart.
2.

Myocardium Consist of thick bundles of cardiac muscle Contracts Endocardium thin, glistening sheet of endothelium that lines the heart chambers.

3.

41

CHAMBERS OF THE HEART

4 CHAMBERS: 1. ATRIA (2) Receiving chambers Not important in the pumping activity Blood flow is under low pressure
2.

Wednesday, June 20, 2012

VENTRICLES (2)

inferior, thick-walled Discharging chambers Contraction propulsion of blood circulation

42

Wednesday, June 20, 2012

VALVES: Allow the blood flow in only one direction through the heart chambers. 1. ATRIOVENTRICULAR VALVES Between the atrial & ventricular chambers on each side. Prevents the backflow of blood into the atria during ventricular contraction. Bicuspid valve mitral valve (left) Tricuspid valve right AV Chordae tendinae anchor the AV valve flaps in a closed position Open during heart relaxation & closed ventricular contraction.

43

Wednesday, June 20, 2012

2.

SEMILUNAR VALVES Guards the bases of the two large arteries Pulmonary & aortic semilunar valves Closed during heart relaxation & open during ventricular contraction.

44

UNoxygenated blood enters the atrium on the right side of the heart. Unoxygenated blood comes in from the top of the body through the superior vena cava.
Unoxygenated blood comes in from the lower body though the inferior vena cava.

45

Wednesday, June 20, 2012

Wednesday, June 20, 2012

While the unoxygenated blood is in the right atrium, the tricuspid valve is closed to keep the blood from flowing down to the ventricle.

46

Wednesday, June 20, 2012

The atrium contract s and the tricuspid valve opens, forcing the blood down into the ventricle

47

The tricuspid valve closes again so that blood cannot move back up into the atrium.

48

Wednesday, June 20, 2012

The ventricle contracts. This forces the unoxygenate d blood through the pulmonary valve and into the pulmonary arteries.

49

Wednesday, June 20, 2012

The right pulmonary artery takes the unoxygenated blood to the right lung.
The left pulmonary artery takes the unoxygenated blood to the left lung.

Wednesday, June 20, 2012

THE PULMONARY ARTERIES ARE THE ONLY ARTERIES THAT CARRY UNOXYGENEATE D BLOOD.

50

In the lungs, the carbon dioxide in the blood diffuses into the alveoli.
The oxygen in the lungs diffuses into the blood.

Wednesday, June 20, 2012

This is called gas exchange.

http://www.webmd.com/hw/health_guide_atoz/tp10237.asp
51

Oxygenated blood from the lungs enters the heart through the left atrium.
The mitral valve is closed to keep the blood from going into the ventricle.

52

Wednesday, June 20, 2012

Oxygenated blood from the right lung returns to the heart through the right pulmonary vein. Oxygenated blood from the left lung returns to the heart through the left pulmonary vein.

Wednesday, June 20, 2012

THE PULMONARY VEINS ARE THE ONLY VEINS THAT CARRY OXYGENATED BLOOD.

53

The left atrium contracts. This forces the oxygenated blood through the mitral valve into the right ventricle.

54

Wednesday, June 20, 2012

Wednesday, June 20, 2012

The mitral valve closes again. This keeps the oxygenated blood from moving back up into the atrium.

55

Oxygenated blood is forced into the aorta to be carried to the rest of the body.

56

Wednesday, June 20, 2012

Wednesday, June 20, 2012

Oxygenated blood is carried to all body cells where oxygen diffuses into the cells and carbon dioxide diffuses into the blood. Blood carrying carbon dioxide then returns to the heart.

57

Wednesday, June 20, 2012

And the cycle begins again.

58

MEANWHILE

While the blood is moving oxygen and carbon dioxide around, it is also moving nutrients, other wastes, hormones, and antibodies at the same time.

Wednesday, June 20, 2012

59

CORONARY ARTERY DISEASE

It is a heart disease due to impaired coronary blood flow disrupts the blood rich oxygen and nutrients for metabolism

Most common cause is ATHEROSCLEROSIS

60

ETIOLOGY: Non- modifiable Factors: Age Gender Family history Modifiable Factors: Hyperlipidemia Hypertension Cigarette smoking Diabetes mellitus Physical inactivity Obesity

61

ATHEROSCLEROSIS

Abnormal deposit of fatty substances and fibrous tissue in the intima of the blood vessel.

62

ATHEROSCLEROSIS
PATHOPHYSIOLOGY: Injury in the endothelial lining Allows entry of lipids to the intima Recruits monocytes and promote expression of inflammatory mediators Monocyte differentiate macrophages and ingest LDL

63

fatty streak or foam cells formation

Stimulates release of growth factors Fibrous plaque formation Foam cells increases in size becomes rigid, calcified and fragile Intimal ulceration

64

Platelet aggregation further increasing the plaque

Narrowing of blood vessel lumen

Obstruction of blood flow No or decrease blood supply

65

ANGINA PECTORIS

Clinical syndrome usually characterized by episodes of pain and pressure in the anterior chest. Increase O2 demand and decrease O2 supply. Usually a result of atherosclerosis.

66

Types of angina pectoris: 1. Stable angina a consistent pain that occurs on activity and is relieve by rest.
2.

Unstable angina increasing in frequency, duration and intensity of pain at lower level of activity. Prinzmetal angina result of coronary vasospasm Silent angina ischemia occurs without at all
67

3.

4.

Clinical Manifestations: a. Pain b. Shortness of breath c. Diaphoresis d. Pallor e. Weak or numbness of arm f. Dizziness or lightheadedness g. Feeling of impending doom h. Choking or strangling sensation i. Anxiety

68

Diagnostic tests: 1. ECG 2. 2D echocardiogram 3. Cardiac enzymes 4. CBC, ESR 5. Lipid levels 6. Exercise Stress Test 7. Cardiac catheterization & angiography

69

Medical management: 1. Oxygen therapy 2. Pharmacological treatment:

a. b. c. d. e.

Nitrates Beta-adrenergic blocker Calcium channel blocker Antiplatelet drugs Antilipidemics

70

3. SURGICAL MANAGEMENT
A.

CABG

71

72

B. PTCA

73

C. Laser angioplasty - atherectomy

74

Nursing Management: 1. Lifestyle modification 2. Careful monitoring during anginal episodes 3. Keep nitroglycerin available for immediate use. 4. Complete bed rest 5. Provide stress reduction activity

75

MYOCARDIAL INFARCTION
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Coronary occlusion, heart attack, & MI are used synonymously, but the preferred term is MI. characterized by the ischemic death of the myocardium due to the reduced of absence of blood flow.

76

CAUSES: 1. Atherosclerosis
1.

Complete occlusion of an artery by an embolus or thrombus Vasospasm of a coronary artery (constriction or

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2.

narrowing)

3.

Decreased oxygen supply (acute blood loss, anemia, or

low blood pressure)

5.

Increased demand for oxygen (from rapid HR,

thyrotoxicosis, or ingestion of cocaine)

oxygen supply & demand.

Result: Profound imbalance exists between myocardial

77

PATHOPHYSIOLOGY:
occlusion/vasospasm
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decreased diameter of the arterial wall

reduced/decreased blood supply decreased oxygen supply to the myocardium NECROSIS

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CLINICAL MANIFESTATIONS:
1.

Sudden & persistent chest pain (despite rest &

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medication is the primary presenting symptom)

Anxious & restless Cool, pale & moist skin Tachycardia & tachypnea Epigastric pain Disorientation & confusion Fainting & weakness

2.
3. 4.

5.
6. 7.

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DIAGNOSTIC EVALUATIONS:
1. 2.

3.
4. 5.

ECG 2D echocardiogram Coronary angiography Myocardial perfusion imaging with thallium-201 Serial serum cardiac markers:

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a. b. c. d.

Creatine kinase (CK) Lactic dehydrogenase (LDH) Myoglobin Troponin T & I

80

Cardiac enzyme

Normal value

with Acute Myocardial Infarction onset peak Duration 46 days

Troponin

0 ng/ml (> 1.5 ng/ml is dx for MI) 96 140 IU/L (F) 38 174 IU/L (M)

3.5 7 hrs

CPK

4 6 hrs

12 - 24 hrs

3-4 days

CPK MB SGOT LDH

0 6 18 IU/L (F) 7 21 IU/L (M) 70 180 mg/dl

24 48 hrs 12 18 hrs 24 48 hrs

12 24 hrs 24 48 hrs 3 6 days

23 days 3-4 days 710 days

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MEDICAL MANAGEMENT:
Goals: reperfusion of the necrotized area
a. b.

c.

To minimize myocardial damage To preserve myocardial function Prevent complications Oxygen therapy Pain control

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1. 2.

Opiate analgesic
a. Morphine sulfate (DOC)

Vasodilator
a. Nitoglycerine

Anxiolytic therapy
a. Benzodiazepine
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3.

Other pharmacologic therapy

Thrombolytics to dissolve & lyse the thrombus in the coronary artery (thrombolysis) allowing blood flow through the coronary artery Do not affect the atherosclerotic lesion. Must be administered ASAP after the onset of symptoms that indicate an AMI.
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a.

Streptokinase increases the amount of plasminogen activator thus increasing the amount of both circulating & clot-bound plasminogen. Made from bacteria (risk of allergic reaction) Vasculitis is noted up to 9 days after adminstration. Not used if the patient received streptokinase in the past 6-12 83 months.

b.

Tissue Plasminogen activator (t-PA) activates the plasminogen on the clot more than the circulating plasminogen. Heparin can be used (to prevent another clot from formingh

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at the same lesion site because t-PA dose not decrease the clotting factors)
Anticoagulants/antiplatelet Beta-adrenergic blockers Antidysrhythmics ACE inhibitors Surgical management PTCA CABG

4.

84

NURSING INTERVENTIONS:
1.

Relieving chest pain.

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2.

Improving respiratory function. Promoting adequate tissue perfusion. Reducing anxiety. Managing & monitoring potential complications

3.

4.

5.

85

CARDIAC

TAMPONADE

is a rapid, unchecked increase in pressure in the pericardial sac compressing the heart, impairing the diastolic filling, reducing cardiac output

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CAUSES: 1. Effusion 2. Hemorrhage due to trauma 3. Hemorrhage due to nontraumatic causes 4. Chronic renal failure 5. Connective tissue disorder 6. Acute myocardial infarction

86

PATHOPHYSIOLOGY:
accumulation of fluid in the pericardial sac compression of the heart chambers
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obstruction of blood flow into the ventricles

increase pressure in the pericardial sac decreased venous return reduces the amount of blood that can be pumped out reduced cardiac output
87

CLINICAL MANIFESTATIONS:
1.

Feeling of fullness within the chest ( from stretching of the

pericardial sac) pressure)

2. 3.
4. 5. 6. 7. 8. 9. 10.

Elevated CVP with jugular vein distention (increased venous

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Shortness of breath Pulsus paradoxus Muffled heart sounds Narrowed pulse pressure Orthopnea Diaphoresis anxiety & restlessness Cyanosis Weak, rapid peripheral pulses
88

DIAGNOSTIC TEST:
1. 2. 3. 4.

Chest x-ray ECG Echocardiogram CT scan or MRI

MEDICAL MANAGEMENT: Goal: to relieve intrapericardial pressure & cardiac compression 1. Pericardiocentesis 2. Pericardiotomy 3. Insertion of a drain into the pericardial sac 4. Inotropic drugs 5. Blood transfusion 6. Protamine sulfate (heparin-induced tamponade) 89 7. Vitamin K administration (warfarin-induced tamponade)

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NURSING RESPONSIBILITIES:
1. 2. 3. 4. 5. 6. 7. 8. 9.

Monitor the cardiovascular & hemodynamic status frequently. Monitor for pulsus paradoxus. Watch closely for signs of increasing tamponade, increasing dyspnea, & arrythmias. Infuse IV solutions & inotropic drugs. Administer oxygen therapy. Monitor respiratory status. Prepare for pericardiocentesis or thoracotomy. Assess renal function status closely. Monitor capillary refill time, LOC, peripheral pulses, & skin temperature for evidence of diminished tissue perfusion.

90

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CARDIOGENIC SHOCK

occurs when the heart cannot pump enough blood to supply the amount of oxygen needed by the tissues.

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impairs tissue perfusion

CAUSES: 1. Myocardial infarction (most common) 2. Myocardial ischemia 3. End-stage cardiomyopathy 4. Myocarditis 5. Depression of myocardial contractility 6. Prolonged cardiac dysfunction 7. Acute mitral or aortic insufficiency 8. Ventricular septal defect
91

PATHOPHYSIOLOGY:
decreased contractility
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decreased cardiac output

Myocardial ischemia

hypoxia
pulmonary pressure
pulmonary blood volume decreased BP
92

decreased coronary artery perfusion

CLINICAL MANIFESTATIONS:
1. 2. 3. 4. 5.

6.
7. 8. 9. 10.

Restlessness, confusion & agitation Low blood pressure Rapid & weak pulse Cold & clammy skin Rapid, shallow respirations Increased respiratory crackles Hypoactive bowel sounds Oliguria Narrowing pulse pressure Dysrhythmias

93

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DIAGNOSTIC TESTS:
1. 2.

3.
4. 5. 6.

Pulmonary artery pressure monitoring ABG ECG Echocardiography Serum cardiac enzymes Cardiac catheterization

94

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MEDICAL MANAGEMENT:
Goals: to increase cardiac output to improve myocardial perfusion to decrease cardiac workload
1.
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2.
3. 4. 5. 6. 7.

Intubation & mechanical ventilation Supplemental oxygenation Continuous cardiac monitoring Maintaining at least 2 IV lines with large-gauge needles IV fluids, crystalloids, colloids, or blood products Strict bedrest Mechanical assistance: IABP (Intra-aortic balloon pump)

95

7. a. b. c. d. e.

Pharmacological therapy: Vasodilator Vasopressor Diuretics Inotropic drugs Thrombolytics

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NURSING RESPONSIBILITIES: 1. Monitor & record vital signs & peripheral pulses every 5 minutes until stable. 2. Assess the skin color & temperature. 3. Closely monitor PAP, PAWP & cardiac output. 4. Measure CVP. 5. Measure urine & output every through an indwelling catheter. 6. Monitor ABG, CBC & electrolyte levels. 7. Administer medications as ordered.

96

8.

IABP: Move the client as little as possible. Never flex the ballooned leg at the hip. Never place the patient sitting position. Assess pedal pulses, skin temperature & color. Check the dressing over the insertion site for bleeding.

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CONGESTIVE HEART FAILURE:

Is the inability of the heart to pump enough blood to meet the metabolic needs of the body.

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Results in intravascular & interstitial volume overload & poor tissue perfusion.
Most commonly occurs with disorders of cardiac muscle that result in decreased contractile properties of the heart. Categories: Left-sided failure Right-sided failure Systolic dysfunction Diastolic dysfunction

a. b. c. d.

98

CAUSES:
1.

Myocardial dysfunction Coronary artery disease Ischemia Myocardial infarction Dilated cardiomyopathy Arterial hypertension Valvular heart disease

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2. 3.

99

ETIOLOGIC FACTORS:
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1.

2.
3. 4. 5.

Increased metabolic rate Hypoxia Anemia Respiratory & metabolic acidosis Cardiac dysrhythmias

100

PATHOPHYSIOLOGY:
1. a. b. c. d.

Myocardial dysfunction CAD Ischemia M.I . Dilated cardiomyopathy

decreased blood flow to myocardium

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hypoxia - - - acidosis necrosis decreased contractility CHF

101

2.

Arterial hypertension

increased workload of the heart

hypertrophy of myocardial muscle fibers decreased contractility of the myocardium decreased ability of the heart to fill during diastole
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increased amount of resistance

102

3.

Valvular heart disease

difficulty of blood in moving forward

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decreased ejection of the blood

increased pressure with in the heart

decreased myocardial contractility

pulmonary & venous congestion

103

Left & right-sided dysfunction : word format

104

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Compensatory mechanisms:

all types of heart failure

reduced cardiac output

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a. b. c. d.

triggers compensatory mechanism at the expense of increased ventricular work Increased sympathetic activity Renin-angiotensin aldosterone system Ventricular dilation Ventricular hypertrophy

105

CLINICAL MANIFESTATIONS:
Left-sided Cardiac Failure: 1. Dyspnea on exertion 2. Paroxysmal nocturnal dyspnea 3. Orthopnea 4. Cough 5. Pulmonary crackle 6. Lower than normal oxygen saturation level 7. Restlessness & anxiety 8. Tachycardia/palpitations 9. Easily fatigued 10. Insomia Right-sided Cardiac Failure: 1. Dependent edema 2. Weight gain 3. Hepatomegaly 4. Distended neck veins 5. Ascites 6. Anorexia & nausea 7. Nocturia 8. Weakness
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106

DIAGNOSTIC EXAM:
1. 2. 3. 4. 5.

Chest x-ray ECG Liver & renal function test ABG Echocardiogram

107

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