Exam 3 part 4 Flashcards
s/s of forward effect of left sided heart failure
decreased CO
- decreased blood supply to tissue
- Fatigue
- Weakness
- Dyspnea
- cold intolerance
- Dizziness
backup effect of left sided heart failure
low ejection fraction 40% or lower, weak cardiac contractions
- Blood backs up into the lungs, increasing pressure; pulmonary edema
s/s of backup effect of left sided heart failure
Related to Pulmonary congestion because of the increased pressure
- Dyspnea and orthopnea
- Coughing with frothy sputum
- Paroxysmal nocturnal dyspnea (severe nighttime shortness of breath) - acute pulmonary edema. - Wakes up gasping for air, coughing up some frothy, blood-stained sputum (hemophysis)
- Rails/crackles
- Harder to inhale
- Cyanosis and signs of hypoxia due to decreased gas exchange and hemoglobin not fully oxygenated
right sided heart failure backup effect
weak contractions, ejection fraction of 40% or lower, blood flows back toward the extremities and internal organs causing edema
right sided heart failure backup effect s/s
- Edema in feet/legs
- Hepatomegaly, splenomegaly impaired liver and spleen function
- Ascites
- Distended neck veins
right sided heart failure forward effect s/s
same as left side
decreased CO
- decreased blood supply to tissue
- Fatigue
- Weakness
- Dyspnea
- cold intolerance
- Dizziness
heart failure compensatory mechanism
- Activate Sympathetic nervous system (tachycardia, pallor, tachypnea - deliver oxygen to tissues so they don’t die)
- Activation of renin-angiotensin system (increased thirst and less peeing during the day - oliguria)
- release AII (vasoconstriction)
- release ADH (pee less)
- release Aldosterone (Na and water retention)
right sided heart failure causes
pulmonary hypertension
pulmonary valve stenosis
pulmonary disease
left sided heart failure causes
Systemic hypertension
Aortic stenosis
left ventricular infarction
main cause of heart failure
left ventricular infarction
Diagnosis of heart failure
- Establishing the cause and extent of cardiac dysfunction
- based on s/s patient presents with
- Patient history
- BNP levels (100 pg/mL +)
Hypovolemic shock
- Loss of whole blood
- Loss of plasma
cardiogenic shock
The heart fails to pump blood adequately.
- Decreased cardiac output lowers BP.
- The sympathetic system responds.
- Vasoconstriction increases resistance to blood flow.
- Increased workload on the heart worsens heart failure
cardiogenic shock cause
- MI
- Acute valve damage, ventricular septal defect
- Sustained arrhythmias
obstructive shock
Inability of heart to fill - cardiac tamponade
distributive shock
- Blood vessels dilate.
- Not enough blood to fill the circulatory system.
- Blood flow decreases.
- Less blood is returned to the heart.
- Less blood is circulated to the body
Causes of Distributive Shock
Decreased sympathetic activity: neurogenic
- Brain or spine injury; anesthetics; insulin shock; emotion
Vasodilator substances in blood
- Type I hypersensitivity (anaphylactic shock)
- Inflammatory response to infection (sepsis)
Vessel damage from severe hypovolemia
- loss of sympathetic tone (neurogenic shock)
septic shock
due to systemic infection
- Inflammatory mediators released into the circulation
- Cause systemic signs of inflammation
- Activate pathways
(Coagulation, complement, fibrinolytic)
Anaphylaxis
Systemic response to the inflammatory mediators released in type I hypersensitivity
- Histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation.
- bronchoconstriction
cardiac effusion
Fluid accumulates in the pericardial sac slowly, no symptoms, heart adjusts
cardiac tamponade
Fluid accumulates rapidly, causing pain and compressing the heart, making it unable to fill
ventricular septal defect
- Hole in septum between two ventricles (left is thicker than right)
- When blood comes from left atria into left ventricle and blood goes through defect between vents
- All blood entering circulation is fully oxygenated, but there is less of it
LEFT TO RIGHT
Tetralogy Fallot
all 4 defects at birth must occur
1 - VSD
2- pulmonary stenosis
3 - right ventricular hypertrophy (wall of right vent is thicker than left
4 - over riding aorta - aorta closer to septum and ventricular septum defect
RIGHT TO LEFT
Acyanotic condition
VSD - all of the blood that is entering systemic circulation is fully oxygenated
Cyanotic condition
Tetralogy Fallot - When heart contracts, blood moves from right side to left side into aorta, so the blood doesn’t go to the lungs and
Doesn’t get oxygenated (blood is mixed oxygenated and deoxygenated)
What are cardiac enzymes and how are they used
Troponin, myoglobin, CK - raises in these enzymes signify that there has been an MI. the higher the level, the more
cardiac damage has occurred
What is BNP and how is it used
Brain natriuretic peptide. Used to diagnose heart failure, evaluate the effectiveness of treatment, and evaluate the severity of the heart failure. Level of BNP will lower if treatment is effective
paroxysmal nocturnal dyspnea
Acute pulmonary edema
- Pt wakes up gasping for air, coughing up frothy, blood-tinged sputum (hemphysis)
who would you expect to see paroxysmal nocturnal dyspnea in
Left sided heart failure patients
Why do people suffering from heart failure suffer from hypervolemia?
Blood isn’t being pumped efficiently, so it pools in the lungs and the extremities. Kidneys are also triggered to retain sodium and water, further increasing the volume
Dromotropic effects of cardiac medications
Cardiac conduction - how fast are the action potentials moving through the system? (neg = decreased conduction velocity)
inotropic effects of cardiac medications
Force of ventricular contraction
- Positive inotropic - greater force of contraction
- Negative - weaker force of contraction
Chronotropic effects of cardiac medications
Heart rate
- Negative - slows it down
- Positive - speeds it up
What virus causes AIDS
Human immunodeficiency virus
what are some s/s and associated illnesses seen in AIDS
patients?
- Opportunistic infections
– Respiratory: pneumocystis pneumonia, pulmonary TB
– Gastrointestinal: esophageal candidiasis, CMV, herpes simples esophagitis
– Nervous system - Malignancies - Kaposi sarcoma, non-Hodgkin’s lymphoma
- Wasting syndrome: involuntary weight loss of >10% of starting weight, diarrhea, chronic weakness and fever
- Metabolic disorders: insulin resistance and diabetes, lipodystrophy (abnormal fat loss or accumulation), hyperlipidemia and mitochondrial disorders
What is the difference between being diagnosed HIV positive and being
diagnosed with AIDS
T helper cell count goes below 200
primary immunodeficiency
Genetic
- Humoral (B-cell) deficiencies - hypogammaglobulinemia
- Cellular (T-cell) deficiencies - thymic aplasia
- Severe combined immunodeficiency disorder (SCID): deficient in B and T Cell due to non-functional - T-helper cells. bubble boy disease
- Wiskott-Aldrich syndrome: production of abnormal or nonfunctional immune cells - decreased antibody production
secondary immunodeficiency
Acquired—consequence of another event
- Malnutrition
- Immunosuppressant drugs
- AIDS
- Kidney disease
- Hodgkin lymphoma
- Chemotherapy
MI treatments
- rest, oxygen therapy and analgesics
- anticoagulants
- thrombolytic agents (dissolve the clot, given within first hour)
– first hour - streptokinase, urokinase, tissue plasminogen activator (followed by low does aspirin or anticoagulants - warfarin) - Low dose ASA therapy
- Coronary bypass surgery
- Percutaneous coronary intervention
angina treatments
- Nitroglycerin
- Directed toward symptom relief
- Life style changes
- Drugs (decrease workload of the heart)
– Nitrates - increase diabetes of coronary vessels which increases blood flow to myocardium
– Beta blockers
– Calcium channel blockers
how is aging is associated w the development of hypotension
- Decreased thirst reflex, decrease in blood volume
- Decreased baroreflex - supposed to cause vasoconstriction, increased heart rate, increased force of cardiac contraction
- Autonomic nervous system dysfunction - baroreflex doesn’t react quickly enough to postural changes
Blood pressure regulation - renin-angiotensin-aldosterone pathway and what stimulates the activation of the pathway
Heart failure and shock (hypoperfusion of tissues and organs) activate the pathway - pathway raises blood pressure to increase tissue perfusion
What compensatory mechanism occurs in the heart in patients suffering from hypertension or aortic valve stenosis that helps to maintain cardiac output
Increased afterload (force that heart generates to open up aortic valve)
