U5

Question 1

Hypotension

Answer 1

Hypotension: Low blood pressure below 90 Systolic.
Caused by:
Low Fluid volume (Hypovolemia)
Prolonged immobilization
Medications (name some!?!?)
Neurological disease/damage
S/S: lightheadedness, dizziness, fainting (syncope), pallor, diaphoresis, visual disturbances
Severe: Will cause heart attack and Death
Treatment: Fluid bolus (see “Fluid Challenge” below, blood transfusion or fluid volume expanders as needed (see “Shock” further down in the outline).

Question 2

Fluid Challenge

Answer 2

“FLUID CHALLENGE” Rule of Thumb: Replace one liter of fluid for each
10 point drop in systolic pressure or 10 point rise in heart rate

Question 3

Orthostatic Hypotension

Answer 3

Orthostatic (postural) Hypotension: A decrease in both Systolic B/P & Diastolic B/P on standing from a reclining position (there must be at least a 10 point drop in the systolic pressure to be considered an orthostatic change.) Heart rate is often more sensitive than blood pressure changes and will increase to compensate for low blood volume. Normal or compensatory vasoconstrictor response on standing is replaced by marked vasodilation (which leads to blood pooling in the muscle vasculature & renal beds).

Question 4

How to do Orthostatic B/P reading:

Answer 4

How to do Orthostatic B/P reading: Take blood pressure lying down FIRST,
then have patient SIT for second B/P reading
then have patient STAND for third B/P reading

Question 5

Vasovagal Hypotension

Answer 5

Vasovagal hypotension: A reflex of the involuntary nervous system that causes the heart to slow down (bradycardia) which in turn affects the nerves to the blood vessels in the legs permitting those vessels to dilate. As a result the heart puts out less blood, the blood pressure drops, and what blood is circulating tends to go into the legs rather than to the head. The brain is deprived of oxygen which causes fainting.

Question 6

S h o c k (always causes HYPOtension)

Answer 6

Hypotension is most often due to HYPOVOLEMIA →
Hypovolemia (low volume) causes POOR PERFUSION →
Poor Perfusion means blood is not getting into body tissues so…
OXYGEN is not delivered → Organs stop functioning and body DIES

Question 7

Compensatory stage of shock

Answer 7

Compensatory—
Mechanisms are activated to maintain perfusion to heart and brain (epinephrine and norepinephrine are excreted to activate the “Fight or Flight” part of the Adrenergic Nervous System. Review Stress & Adaptation from Unit 2 (Integrative Body Systems) if needed.

Question 8

Progressive stage of shock

Answer 8

Progressive stage-
Begins as compensating mechanisms fail to maintain homeostasis. Tissues become hypoxic because of poor perfusion.
Cells switch to anaerobic metabolism → lactic acid builds up and produces metabolic acidosis. Also, cells die/break open/release potassium which compounds acidosis.
Depressed myocardial function → hypoxia which then promotes the release of endothelial mediators. These chemical mediators cause VASODILATATION and endothelial abnormality leading to venous pooling and increase CAPILLARY PERMEABILITY—increase risk of DIC (see Unit 3 – Hematologic System).

Question 9

Irreversible/ refractory stage of shock

Answer 9

Irreversible/refractory-
Permanent organ damage occurs—leads to cell death. Hypotension results from increased capillary permeability. Lactate (lactic acid) builds up due to anaerobic metabolism, so a HIGH Lactate level (blood test) is an indicator of POOR prognosis (outcome) for the patient.
Circulatory and respiratory failure occurs - death is inevitable

Question 10

“3 Second Assessment” – a complete head-to-toe rapid assessment of all major body systems in 3 seconds!!!

Answer 10

Using this model to assess a patient will help you keep your priorities straight. ALSO A VERY USEFUL WHEN TAKING A TEST!

Airway/Breathing: look for chest rise. If present, the person has an open airway and is ventilating adequately.

Cardiac/circulation: feel radial pulse. If present then person has at least an 80 systolic B/P which is adequate to
perfuse the brain. Note dysrhythmias; character of pulse (weak or bounding). Feel temperature & moisture on skin.

Deficit of NEURO functions: Ask person to move feet. This assesses the acoustic nerve; the ability of the brain
to process information; brain’s ability to send a signal down the spinal cord; & ability of the spinal cord to send
nerve impulses to the most distal nerves in the body (feet). If everything works, the person is neurologically intact

Question 11

Causes (types) of Shock

Hypovolemic

Answer 11

Hypovolemic: Deficient circulating vascular volume (hemorrhage)

Question 12

Causes (types) of Shock

Cardiologic

Answer 12

Cardiogenic (Obstructive) Secondary to heart failure
Inability of the heart to fill properly (pericarditis)
Obstruction to outflow from the heart (PE, Pneumothorax, Hemothorax, dissecting aneurysm
Pump failure

Question 13

Causes (types) of Shock
Septic
Anaphylactic
Neurogenic

Answer 13

Distributive: septic, anaphylactic, neurogenic - Altered regulation of vascular tone
~ SEPTIC SHOCK: Infection commonly caused by Gram negative bacteria toxin → massive vasodilation ~ ANAPHYLACTIC SHOCK: Overwhelming immune response (vasodilation) to an allergen
~ NEUROGENIC SHOCK: Loss of blood vessel tone, → displacement of the vascular vol. away from the
heart & central circulation. Example: Spinal Shock - Spinal Cord Injury

Question 14

Hypertension

Answer 14

Hypertension = B/P consistently higher than 140/90

1 in 3 American adults have high blood pressure. Known as the “Silent Killer” because there are minimal S/S in most people who have hypertension [HTN].

Question 15

ARTERIOSCLEROSIS

Answer 15

• Arteriosclerosis – An INFLAMMATORY PROCESS that causes abnormal thickening and hardening of arterial wall from deposition of collagen into vessel wall leads to diminished distensability

Question 16

ATHEROSCLEROSIS

Answer 16

• Atherosclerosis - is the narrowing of the artery because of plaque build-up. It is a form of arteriosclerosis resulting from fat being deposited in vessel wall that reduce lumen size.

Question 17

Steps of Atherosclerosis Development in a Blood Vessel

Answer 17

1: Ulceration of vessel - Vessel injury can be due to inflammation, high blood pressure, infections, etc.

Question 18

Venous Disorder

Varicose Veins

Answer 18

Varicose veins
Etiology: gravity, increased abdominal pressure, valve incompetence
Incidence: Risk factors include prolonged sitting; pregnancy.
Pathophysiology: venous pooling –> distended vein –> edema and further engorgement
S/S: primary - appearance; secondary - edema, tired, aching legs
Rx: improve venous return, sclerosis, and ligation

Question 19

Venous Disorder

Deep Vein Thrombosis

Answer 19

DEEP VEIN THROMBOSIS (DVT) (Note: There are some decent short YouTube videos available if you need a more thorough explanation of the process)
Etiology: diminished blood flow (especially in the legs) and pressure
RISK FACTORS: Prior history of a DVT (this is the #1 highest risk factor); Pregnancy;
sitting for long periods (i.e., driving/flying); desk job; Birth control pills; obesity; smoking.
Pathophysiology: hemostasis –> activation of intrinsic clotting cascade –> thrombus formation that is the source of blood clots that break off and travel to different parts of the body (emboli) – usually to lungs and causing P.E. (pulmonary emboli).
S/S: tenderness, swelling, redness/warmth in affected leg (when compared to other leg)
Rx: anticoagulants (like Heparin, Coumadin, Plavix or Lovenox) and prevention (What are the MODIFIABLE R.F.’s)

Question 20

Arterial Disorder

Peripheral Arterial Occlusive Disease

Answer 20

1 - Peripheral Arterial Occlusive Disease (PAOD) - caused by atherosclerotic blockages in the LARGE arteries like carotid and femoral (not smaller arteries coronary, aortic arch, brain). S/s begin to show when artery is 50% occluded.
S/s – refer to Venous vs. Arterial chart above.

     Most common symptom is “Claudication” also referred to as “Intermittent Claudication.” Whether a patient progresses to limb amputation largely depends on the number and severity of cardiovascular risk factors (ie, smoking, hypertension, or diabetes). Continued smoking has been identified as the adverse risk factor most consistently associated with the progression of PAOD.

Claudication, (defined as reproducible ischemic muscle pain) is one of the most common S/S of peripheral arterial occlusive disease (PAOD) caused by atherosclerosis. Claudication occurs during physical activity and is relieved after a short rest. Pain develops because of inadequate blood flow.

Question 21

Arterial Disorder

Thrombangitis obliterans

Answer 21

2 - Thrombangitis obliterans (BUERGER’S DISEASE)
Etiology: disease of the arteries and veins in the arms and legs - Unknown cause, possibly autoimmune
Incidence: young men who are heavy smokers
Pathophysiology: peripheral arterial inflammation –> thrombus formation/vasospasm–> occlusion
S/S: pain, tenderness, dependent rubor (s/s of inflammation =“SHARP”)
Rx: smoking cessation, vasodilators, amputation

Question 22

Arterial Disorder

Raynaud’s Disease

Answer 22

3 - RAYNAUD’S DISEASE/phenomenon/syndrome (optional video) https://www.youtube.com/watch?v=pjar6pXxQ34 (7:12 min)
Etiology: Possibly Genetics, unknown
Incidence: young women
Pathophysiology: triggers (cold, stress, drugs) –> digital arterial vasospasm –> distal to proximal that causes reduced blood flow to the extremities.
S/S: Fingers turning white after exposure to temperature changes or emotional events; pallor/cyanosis, numbness, cold progressing from distal to proximal part of limb, followed by redness and throbbing pain,
Rx: avoiding triggers, vasodilators (NOTE: Poor circulation in hands, so do not put oximeter on fingers).

Question 23

Coronary Artery Disease (CAD)
Coronary artery disease,(aka, coronary heart disease, or just “heart disease”)
is the #1 killer in America

Answer 23

Etiology: atherosclerosis, vasospasm, thrombi
Incidence: 50% all deaths (35% deaths in 35-65 year old)
Non-modifiable - age > 60, gender especially male, genetic predisposition, Type I Diabetes
Modifiable – hyperlipidemia (high cholesterol), hypertension, smoking, obesity, sedentary lifestyle, Type II Diabetes.
Pathophysiology: coronary artery occlusion –> decreased myocardial perfusion –> myocardial ischemia –> angina –> ischemia persists (> 20 minutes) –> ischemic cells are injured –> injured cells necrosis (Myocardial infarction) –> myocardium scars over dead tissue → dead tissue will not conduct electrical current ➔ NO HEART BEAT! (this results in abnormal EKG readings).

Question 24

Treatment of chest pain

MONA

Answer 24

Morphine
Oxygen
Nitro glycerin
Aspirin

Question 25

5 p’s to assess circulation in a limb

Answer 25

Pain
Polar (cold)
Pulselessness
Parathesia 
Paralysis

Question 26

BNP

Answer 26

• BNP is a substance secreted from the ventricles or lower chambers of the heart in response to changes in pressure that occur when heart failure (either left or right-sided) develops and worsens.

BNP is released into the blood stream when the muscle tissue of the ventricles is stretched (as happens when the heart muscle becomes enlarged as it does in CHF). The level of BNP in the blood increases when heart failure symptoms worsen, and decreases when the heart failure condition is stable.

The BNP level in a person with heart failure – even someone whose condition is stable – is higher than in a person with normal heart function. The most important use of natriuretic peptides is in helping to establish the diagnosis of heart failure (HF) in a patient in the urgent care setting in whom the diagnosis is uncertain.