Theory Review Three PDF

Preview

Summary

Theory Review Three...

Description

Theory Review Three Blood Pressure BP=COxPR CO=Cardiac Output (the relationship between Heart rate and stroke volume) PR=Peripheral Resistance (the resistance of the arteries to blood flow) Therefore…. BP=(HRxSV)xPR Blood pressure is directly influenced by:  Blood volume  Viscosity  Venous return  Heart rate  Force of contraction  Elasticity and health of arteries  Any resistance to blood flow  Narrowing of the lumen of the blood vessel  Sympathetic stimulation  Blood pressure monitoring (baroreceptors, vasomotor control)  Hormones Measurement (systolic/diastolic) Systolic: depends on amount of blood ejected and elasticity of the blood vessel walls Diastolic: degree of peripheral resistance and increased workload on the left ventricle Pulse Pressure The difference between systolic and diastolic pressures (not to be greater than 40) This is an index of vascular aging Mean Arterial Pressure  Average pressure in patients’ arteries during one cardiac cycle. Indicator of perfusion to tissue.  MAP= 1/3 (pulse pressure) +Diastolic pressure  This should be less than 65mmHG Hypertension Chronically elevated blood pressure. The diagnosing doctor will take the blood pressure several time on multiple occasions (appointments) before diagnosing HTN. Silent Disease

1

Risk Factors:  Age  Hormones  African American (onset earlier and average BP is higher)  Family history  CV status  Salt intake (water retention)  Excessive alcohol intake  Obesity  Prolonged stress S/S      

Typically, NONE Headache Fatigue Malaise Morning headache Dizziness

Primary, Essential or Benign HTN  Idiopathic Theories:  Overactive SYMP NS (vasoconstriction)  Inheritance  Renin Angiotensin system Secondary HTN  Results as a secondary issue  Ex: Renal, Endocrine, Cancer, Pre-eclampsia etc  Underlying problem is treated Malignant HTN  Uncontrolled, progressive  Diastolic is higher Hypertension and Coronary Artery Disease What affects heart rate?  Cardio-inhibitory pressoreceptors (baroreceptors)  Cardioaccellerator reflex  Epinephrine  Emotional responses (fear/anger)  Physical exercise  Body temperature  Vasomotor center of the medulla oblongata  Chemical substances (pH)

2

Some thoughts re HTN:  Aware of any other cardiovascular issues (peripheral vascular disease, diabetes etc)  Decrease sympathetics first to decrease peripheral resistance  Avoid long drainage type strokes (move fluid proximally, but into superficial tissue?) PR ROM, Lymphatic drainage  Positioning  Hydro  Avoid compression of the aorta/carotid (baroreceptors)  Assess for CCHF status/monitor bp regularly Medications Diuretics  Act on kidneys to increase urine/decrease blood flow Beta Blockers  Block sympatictic neurotransmitter from synapsing on the heart, decreases heart rate, therefore allowing for longer refill time (Frank-Starling) Glycosides  Alters the sodium/potassium pump within cardiac muscle cells, therefore slow down the heart rate Alpha blockers  Block sympathetic neurotransmitters from synapsing on the smooth muscle of the arterial system or decreases the number of neurotransmitter impulses from the vasomotor center of the brain (decreases PR) Calcium channel blockers  Modifies the uptake and utilization of calcium in the cardiac muscle and smooth muscle cells in blood vessel wall ACE inhibitors  Supresses the production of angiotensin2 by supressing Angiotensin converting enzyme (ACE) Anticoagulants  Reduces the effect of Vitamin K on blood coagulation (heparin/warfarin) Antithrombotics  Prevent platelet aggregation (aspirin) Vasovagal syncope or neurocardiogenic syncope  Overreaction to certain trigger (sight of blood, or distress)  Heart rate and blood pressure drops suddenly, causing decreased blood flow to the brain and briefly losing consciousness  Caution with direct work with psoas,  Sideline Orthostatic hypotension (postural Hypotension)  Abnormal drop in blood pressure with change in position.

3



Caused by a decrease in venous return to the heart due to pooling of blood in the lower part and inadequate circulatory reflexes.

Causes:  Decreased blood volume  Drug induced hypotension (hypertensive medications, diuretics, antidepressants)  Altered vascular responses or causes of neurogenic origins (ageing, bedrest, ANS dysfunction) Aggravated by:  Heat  Humidity  Heavy meals  Exercise Treatment protocols:  Gradual ambulation to allow circulatory system to adjust.  For example: have patient move into their side for a few moments to adjust, then to a sitting position, then to a standing position, waiting a few moments between.  Utilize the “calf pump”  No diuretics/caffeine prior to treatment Coronary Artery Disease  Atherosclerosis (atheromas)  Angina Pectoris  Myocardial Infarction Atherosclerosis  Deposition of fibro-fatty lesions in the walls of the large arteries  Elasticity is lost, walls become thick, and lumen narrows (may obstruct)  Ischemia, infarct, occlusion  High risk individuals: cholesterol levels Cholesterol  Fatty, wax like material used by the body to help construct cell membranes and is essential to brain and nerve function Lipoprotein=cholesterol and its transport protein HDL- high density lipoprotein  “good” lipoprotein, transports cholesterol away from the peripheral cells to the liver (catabolism and excretion) LDL-low density lipoprotein  High lipid content, low protein. Transports lipids from liver to cells. Major contributing factor in atheroma development Atheroma  Endothelial injury in artery, which causes inflammation

4

   

Wbc infiltrate the intima, and in the media (muscle layer). The smooth muscle then proliferates, and a plaque forms Thrombus forms, further decreasing the lumen Atheromas damage the blood vessel wall (higher risk for aneurysm formation, or calcification)

Angina Pectoris Latin for angere-to choke  not a disease, a symptom of coronary artery disease  Intermittent ischemic attacks of the myocardium  Other examples  TIA  Intermittent claudication  Majority caused by atherosclerosis  Other: stenosis, scarring or vasospasm Stable Angina  Attacks only occur when heart needs more oxygen Unstable Angina  May occur when person is at rest Pain distribution pattern  Similar to pectoralis major/minor trigger point referral, and myocardial infarction  Chest wall (upper ½)  Left arm and shoulder  Left neck and jaw  Maybe right sided in some individuals  Tight squeezing feeling under the sternum Signs and symptoms dissipate with decrease in metabolic need Medications-Nitroglycerin  Taken at the beginning of an attack  Sublingually: vasodilates blood vessels Patch: Administers medication constantly **Modifications for treatment…. Possible Precipitators of attack  Overexertion, sudden physical exertion  Emotional stress  Large scale temperature changes  Smoking  Eating large meals  Reaction to medications

5

Modifications for treatment?  Case history intake! (frequency and severity, precipitators, medication protocol)  If attack develops during treatment Stop the treatment Do what is appropriate regarding medications Position supine with trunk elevated, or seated comfortably Monitor, stay calm Heart Attack and Congestive Cardiac Failure Myocardial Infarction Occurs when a coronary artery is totally obstructed, leading to prolonged ischemia or cell death. Infarction can occur by: 1. Thrombus obstructing an artery 2. Vasospasm with a partial occlusion 3. Thromboembolism The majority of myocardial infarctions occur in the left ventricle  With cell destructions, specific enzymes are released (blood test)  Severity of MI depends on size and importance of vessel affected. (think proximal vs distal)  Range from minor to massive  Men survive their first heart attack more than women due to difference in symptom presentation  Risk of fatality increases with subsequent MI  Majority affect left ventricle Risk factors:  Pre-existing heart disease, previous heart attack, angioplasty, bypass surgery or angina  Age, family history  Smoking  High LDL levels, low HDL levels  Overweight, obesity  Physical inactivity  Diabetes  Race: African American more susceptible than Caucasian  STRESS  Alcohol Consumption Prodromal Signs/Symptoms S/S of SNS activation  Cold, clammy, sweaty  Anxiety  Shaking, rapid, shallow breathing

6

 Pallor, cyanosis (lips, fingertips)  Rapid, “thready” pulse  Nausea, digestive disturbances S/S of reduced blood flow to the brain  Light headedness, dizziness, confusion, mental “fog”  Difficulty articulating  Emotional liability, irritability, denial.  Hypotension, weak and rapid pulse, blurred vision, headache etc. Pain pattern  Diffuse and varied presentations  Left shoulder and arm (possibly the right)  Diffuse chest pain  Possible neck and jaw pain  May center on an old injury  Heartburn-like pain Call 911 MI onset  full body tonus  Crushing sub sternal pain  Acute S/S of shock (including vomiting and incontinence)  Loss of consciousness  Women can experience less of the crushing type of pain, but flu/indigestion type of pain, therefore harder to identify and diagnose After stability has been established... Case history questions When? Precipitating factors 1st? If not… others? Meds, then and now Severity Complications ADL’s... And doctor directed instructions Stress levels? Reason for MT and perceptions of MT. TX adaptations  CCHF status  Complications re MI  Medications (antihypertensive, antidepressants, anticoagulants, analgesics, etc.)  Compliance factors  Angina? Complications that may arise….  Myocarditis

7

    

CHF Cardiac dysrhythmia Mural wall thrombosis Mural rupture Valve dysfunction

Heart Failure  Cardiovascular system is highly adaptable, therefore can be complications can be undiagnosed for long periods of time.  Heart failure is the term used to describe weakness or failure of the heart in its function as a pump, due to excess stresses, either intrinsically or extrinsically.  This causes impaired tissue nutrition, waste removal, blood filtration, re oxygenation Acute heart failure is the immediate failure or heart death i.e. massive myocardial infarction or pulmonary embolism Chronic Congestive heart failure is a progressive failure of the heart. This may be due to a problem (stress) caused by the heart itself (myocardial infarction or septal defect), or other demands on the heart (hypertension, respiratory conditions)  Depending on the cause, one side of the heart generally fails first, followed by the other side. (Right vs left failure) Possible stressors to the heart: Intrinsic:  Wall or septum defect (leakage into adjacent chamber)  Valve dysfunction  Heart beat regulation problems  Heart wall infarction  Heart strength/health/fitness  Ischemic states (coronary artery disease) Extrinsic  Hypertension  Chronic respiratory conditions  Malnutrition  Obesity  Anemia  Smoking  Sedentary life style  Liver/kidney disorder  Endocrine dysfunction  Peripheral vascular disease  Emotional, psychoemotional, physical stresses  Pregnancy  Neuromuscular disorders, especially involving spasticity or rigidity)

8

What happens to the heart when it undergoes stress? (Adaptive changes )  Increase heart rate  Increase chamber dilation (Frank-Starling law)  Myocardial hypertrophy Long term issues with these adaptive changes Increased heart rate  Less time in diastole causes decrease perfusion to the heart  Decreased time for chamber fill/decrease strength of contraction  O2/C02 exchange can be compromised  Increase heart rate stresses heart out more Chamber dilation  Decrease elasticity of the chamber  Exceed stretch capacity parameter of the cardiac cells  Valvular incompetence and regurgitation Myocardial hypertrophy  Decrease elasticity  Decrease chamber size  Difficulty perfusing heart wall  Enlarged heart compresses lungs (increases stress on the heart) Heart failure progression  Sample initial stressor: HTN Signs and Symptoms of CCHF: Shortness of breath  On exertion  Under stress  When lying flat  Awakened at night (episodic nocturnal dyspnea) Hypertension Edema  In extremities  Anasarca  Acites  Hydropericardium  Hydrothorax Poor circulation esp extremities  Cold hands and feet  Cyanosis/Pallor  Trophic changes (skin, hair loss, nail thickening)  Decreased energy  Tires easily, feels weak  Elevated heart rate

9

 

Heart murmur Enlarged Heart (cardiomegaly)

CHF severity indicators: Speed of dyspnea and under what circumstance  Exertion and emotional stress develops first  Inability to sleep lying flat is (moderate-severe)  Dyspnea at rest is consistent with advanced-severe Blood pressure  If stabilized by medication, the stress on the heart is controlled  If not, CHF intensifies  Number of medication can be an indicator of the stress the heart is under  See hypertension chart (Nursing management) Other disorders-severity and management  Diabetes  Respiratory condition  Hyperthyroidism  History of CV conditions (IE MI, valve disease, infections etc) Tissue status  Cool hands and feet-mild CHF  Cyanosis compared to pallor-moderate to severe  Tissue healing delay (moderate-severe) Adult onset Heart murmur Right VS Left Heart failure: Left sided failure causes either pulmonary congestion or a disturbance in the respiratory control mechanisms, which cause respiratory distress. Due to the gradual nature of heart failure, they may not have signs and symptoms. Most common:  Breathlessness/shortness of breath  Exhaustion  Lower extremity edema  Decrease cardiac output Right sided failure occurs in response to left sided failure or result of pulmonary embolism or cor pulmonale (heart failure originating on the right side due to respiratory dysfunction or other respiratory condition –or living at high altitude)  Peripheral edema (pitted edema) or sacral edema  Right upper quadrant pain (visceral congestion)  Cyanosis of the nail beds  Pulmonary disease

10

Treatment considerations for CCHF?  Depends on severity.  Positioning  Supine, sideline (cardiomegaly or pulmonary edema), semi-fowlers  Hydrotherapy: no extremes, aware of percentage of body, hydrostatic pressure, duration  Symp activation (pain, temperature, stimulating tech, full bladder, communication, comfort level)  Less can be more  Self-care: modify (hydro and exercise)  Tissue fragility concerns (healing times, fragile skin, ulcerations)  Avoid increasing venous return modalities Valves and Vessels Valvular Heart Disease Heart murmur  Turbulent blood flow within or between heart chambers, almost always denoting valve dysfunction. The “murmur” is abnormal “noise” heard on specific auscultation of the heart Due to  Valve stenosis, or incompetence: failure for valve to close properly –regurgitates or leak backwards  Prolapse: abnormally enlarged and floppy valve leaflets and balloons backwards which permits regurgitation of blood. Common causes of valve dysfunction:  Hypertension/CCHF  Complication of MI  Rheumatic fever: autoimmune reaction secondary to infection of strep bacteria, after a period of some weeks, antibodies which have developed to fight the infection appear to sense a chemical similarity between the bacteria and heart tissue (valves are particularly aggressively attacked.  Endocarditis  Congenital abnormality

What are the massage treatment concerns?  CCHF status  Adult onset? -some degree of heart failure (not good with CO) Blood vessel conditions  Arteritis: infection or inflammation of an artery  Phlebitis: infection or inflammation of a vein Caused by:

11

    

Infection Inflammatory conditions Hypersensitivity reactions Direct trauma Idiopathic

Phlebitis and phlebothrombosis are common post childbirth, prolonged bedrest or prolonged immobilization of body parts. S/S of arteritis and phlebitis  Local inflammation  Edema  Pain MX concerns  Platelet activation  Medications Temporal Arteritis  Idiopathic, low grade arteritis of the superficial temporal artery  Most common in persons over 50, generally effects men and women equally  Can be bilateral but usually unilateral. S/S  Often none, silent process  Headache, often confused with migraine  Ipsilateral facial pain, numbness or parasthesia  Ipsilateral vision problems varying in severity from blurring to loss of vision in rare cases Mx concerns.  Thrombosis will occur, but is relatively stable due to the slow progressive inflammatory process.  No direct manipulation  As a precaution, palpate the superficial temporary artery in individuals over 50. The therapist should only be able to palpate the pulse, not the artery  Anti-inflammatory and or anti-coagulant medication

Thromboangiitis Obliterans (Beurger’s Disease)  Genetically conditioned hypersensitivity condition to cigarette smoke  Male  Age 19-40  Jewish or Arabic descent  Heavy cigarette smoker Clinical presentation: Beurger’s  Flare ups of acute angiitis affecting the medium sized arteries and veins of the legs, (distal to the knee) and possibly the forearm

12

    

Intensely painful: pain from irritation and ischemia SHARP Risk of thromboembolism Flare up and remission patterns of varying frequency Blood vessel damage

Mx concerns  During flare up: contraindicated, could do modified relaxation work with light cool/cold applications  Medications: anti-inflammatory, anticoagulant, analgesic or muscle relaxants  Reduced sensation due to reduced perfusion to peripheral nerves  Tissue fragility  Look at ADL’s  CV exercise: good warm ups and cool downs, prolonged post exercise tenderness is common. Use Beurger’s exercises Beurger’s exercises 1. Patient lies supine with hips flexed to 45 degrees (feet up on pillows) until the feet blanche. This usually takes 2-3 minutes. 2. Patient then sits up fully (high seated) until blood flow (and color) returns to the feet. This usually takes another 2-3 minutes. 3. Patient lies supine without elevating legs for 2-3 minutes. This process is repeated 4-5 times, 2-3 times daily. Raynauds disease/phenomenon  “attacks” of arteriolar spasm  typically affect the hands, but may involve feet, nose and ears  during an attack the affected part blanches and may become cyanotic  ischemic pain  episodes may last from a few minutes to a few days  appears to be an irritation or over-reaction of sympathetic nervous system function Raynaud’s Disease  Idiopathic, affecting otherwise healthy individuals  Typical sufferer is somewhat more likely to be female  Attacks are not associated with development of thrombosis or ongoing blood vessel or tissue damage  Generally not treated medically, person may use analgesics during an attack Raynaud’s Phenomenon  Is associated with a known cause. 1. Occupational use of vibrating equipment like hydraulic drills or jackhammers.

13

In this context, is often called “white hand”. Avoidance of symptoms/attacks requires compliance to strict limitations of time spent using this type of equipment. 2. Secondary to autoimmune conditions like SLE and sometimes to cancer. In this context, why Raynaud’s Phenomenon develops in some people and not in others is not clear, but a predictable percentage do develop it. Attacks are typically more severe and frequently associated with ongoing blood vessel damage. Thrombosis may be present and trophic changes in supplied tissues may occur. Treatment is often related to managing the causative condition where possible. Anti-inflammatory and anticoagulant medications may be used as well as analgesics. RMT Considerations (for Raynaud’s) 1. Consult with each patient as to their specific attack triggers. Cold exposure is the most common trigger. Avoid cold hydrotherapy and allowing your patient to get too cold (use blankets). Care should be taken with overall hydrotherapy applications; altered vasodilation an...