The cardiovascular system Flashcards
Hypotension
low bp BELOW 90 SYSTOLIC
Causes of hypertension
Low fluid volume (hypovolemia)
prolonged immobilization
medications (diuretics…)
Neurological disease/damage
Signs and symptoms of hypotension
*lightheadedness,
dizziness,
fainting (syncope),
pallor,
diaphoresis,
visual disturbances.
Severe hypotension will cause heart attack and death
Treatment for hypotension
*fluid bolus blood transfusion or fluid volume, expanders
Orthostatic (postural) hypotension
also called postural hypotension
abnormal drop in systolic bp when changing postition from lying down or sitting to a standing position of at least 20 mm hg or diastolic blood pressure of 10 mm hg
Vasovagal response/ hypotension
a reflex of the vagus nerve
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
Results in the heart putting less blood out and the blood pressure drops and what blood is circulating tends to go into the legs rather than the head. the brain is deprived of oxygen which causes fainting
Main characteristics of orthostatic hypotension
-blood pressure drops due to hypovolemia
-tachycardia results in the heart’s attempt to compensate for low b/p
-give IV or oral fluids until low b/p is normal
-treat the cause of hypovolemia
-maintain patient safety (fall precautions)
Main characteristics of vasovagal hypotension
-Blood pressure drops due to stimulation of the vagus nerve
-bradycardia results from stimulation of the parasympathetic system
-self resolving no tx needed
-maintain patient safety (if patient hates needles and might pass out take proper precautions)
Characteristics of SHOCK
Always causes hypotension
-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
-no O2 leads to organs stop functioning and body dies
3 stages of shock
Compensatory stage
progressive stage
irreversible/ refractory stage
Compensatory stage of shock
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)
Progressive stage of shock
Starts because compensating mechanisms fail to maintain homeostasis. Tissues become hypoxic because of poor perfusion
Cells switch to anaerobic metabolism leads to lactic acid begins to build up and produces metabolic acidosis *also cells die/ break open/ release potassium which makes acidosis even worse
Depressed myocardial function leads to hypoxia which then promotes the *release of endothelial mediators. These chemical mediators cause vasodilation and endothelial abnormality leading to venous pooling and increase capillary permeability increase risk of DIC
Irreversible/ refractory stage of shock
Permanent organ damage occurs which leads to cell death. Hypotension results from increase capillary permeability. Lactate builds up due to anaerobic metabolism, so a *HIGH lactate level is an indicator of POOR prognosis
Oliguria or anuria indicate kidney failure due to low perfusion
CIRCULATORY AND RESPIRATORY FAILURE OCCURS DEATH IS INEVITABLE
Signs and Symptoms of SHOCK
-change in level of consciousness (restlessness and irritability due to cerebral hypoxia)
-Tachycardia and tachypnea
-Cool pale (vasoconstriction in limbs in order to squeeze blood to the core)
-Diaphoretic skin (cool/clammy feeling)
-HYPOTENSION
-low urine output (OLGURIA) due to poor kidney perfusion
-Acidosis leads to CNS depression
-HEART DYSRHYTHMIAS due to poor cardiac perfusion
-RESPIRATORY FAILURE due to poor lung perfusion
Treatment for SHOCK
-intubate as needed (airway)
-Give oxygen (breathing)
-cardiac monitoring (circulation)
-maintain perfusion w/ drugs and fluids (CIRC)
-treat underlying cause
TX PRIORITY
-airway: intubation, suctioning
-breathing: oxygen
-cardiac/ circ: Monitor heart, pump fluids to keep adequate B/p
3 second assessment
a complete head-to-toe rapid assessment of all major body system in 3 seconds
Airway/Breathing: look for chest rise. If present, the person has an open airway and is ventilating adequately
Cardiac/ circulation: feel radical 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 pounding). Feel temp and 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; and ability of the spinal cord to send nerve impulses to the most distal nerves in the body.
Hypovolemic shock
Deficient circulating vascular volume (hemorrhage)
Cardiogenic shock
obstructive secondary to heart failure
-inability of the heart to fill properly (pericarditis)
-obstruction preventing “outflow” from the heart
-pump failure
Distributive: septic, anaphylactic, neurogenic
altered regulation of vascular tone
-septic shock: infection caused by gram negative bacteria toxin leads massive vasodilation
-Anaphylactic shock: overwhelming immune response (vasodilation) to an allergen
-Neurogenic shock: loss of blood vessel tone, lead to displacement of the vascular vol. away from the heart and central circulation. EX: spinal shock - spinal cord injury
Hypertension
B/P is consistently higher than 140/90
The vicious cycle
Major cause of hypertension is arterial injury (blood clots) that causes arterial constriction. Narrowed arteries increase the resistance the heart has to pump against. Pressure goes up in the heart because it is pushing so hard to get the blood out. Ironically the forceful blood flow then causes more arterial injury.
Normal BP for adult
100/60 - 120/80
BP categories
Normal
elevated
high bp (hypertension) stage 1
High blood pressure (hypertension) stage 2
Hypertensive Crisis
Normal (bp category)
less than 120 systolic and less then 80 diastolic
Elevated (bp category)
120-129 systolic and less than 80 diastolic
High bp stage one (bp category)
130-139 systolic or 80-89 diastolic
High bp stage 2 (bp category)
140 or higher systolic and 90 or higher diastolic
Hypersensitive crisis (bp category)
higher than 180 systolic and higher than 120 diastolic
Arteriosclerosis
an INFLAMMATORY PROCESS that causes abnormal thickening and hardening of arterial wall from deposition of collagen into vessel wall leads to diminished distensibility
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
Steps of atherosclerosis development in a blood vessel
1 - ulceration of vessel
2 - fatty streak
3 - fibrous plaque
4 - complicated lesion (thrombosis)
5 - thrombus to embolus
Ulceration of vessel
vessel injury can be due to inflammation, high bp, infections, etc
Fatty streak
initial deposit of cholesterol to cover the ulceration in the vessel lining - a “band-aid”
Fibrous plaque
the fatty streak becomes surrounded by collagen and muco-protein matrix leading to protrusion into the vessel that then causes luminal narrowing
Complicated lesion (thrombosis)
the fibrous plaque becomes calcified and penetrates into the vessel’s muscular layer as well as extending into the lumen producing occlusion leading to a thrombus
thrombus to embolus
when the calcified fibrous plaque chip off and float freely through the vascular system it is termed and “embolus” these fragments can block smaller vessels and stop blood flow which could result in everything from localized tissue necrosis to death from a pulmonary embolism that lodges in the lungs
Primary hypertension
etiology (cause) : UNKNOWN (genetic and environmental)
*High risk groups: inherited, race, age, insulin resistance, diet, obesity, alcohol, and smoking
Incidence: ACCOUNTS FOR 90-95% OF HTN
Pathophysiology: hypovolemia, vasoconstricion, resistance in vessels
S/S: USUALLY NONE, morning HA, fatigue,
Rx: DIET, EXERCISE, MEDICATION (LIFE-LONG)
Secondary HTN
Etiology: ATTRIBUTABLE TO ANOTHER DISEASE PROCESS
Incidence: accounts for <5% of HTN
pathophysiology: it has many different causes including ENDOCRINE DISEASES, KIDNEY DISEASES, and TUMORS. it also can be a SIDE EFFECT of many MEDICATIONS
S/S: same as primary HTN and those associated with disease process
Rx: treat underlying cause
CRP is a what
blood test for heart damage and a serum marker for cardiac inflammation
If elevated in the blood it is considered a major risk factor for atherosclerosis and vascular disease
Vascular occlusion
Differentiate ARTERIAL and VENOUS occlusions by manifestations complications and treatment
main factor increasing risk for venous thromboembolism
Prior VTE (most significant risk factor for DVT and PE)
5 P’s
Pain
Pallor- Polar
Pulselessness
Paresthesia
paralysis
Venous Occlusion cause
cause: sedentart, sitting for long periods, bed bound, vessel injury, leads to DVT’s
Venous Occlusion S/S
SHARP
pulse: present
edema: present
color: pink to red
temp: warm to hot
Pain: aching, throbbing
Venous occlusion Tx
Anticoagulant
embolectomy
Arterial occlusion cause
Vasospasm, atherosclerosis, vessel injury
Arterial occlusion S/S
5 P’s
pulse: lower or absent
edema: none
Color: pale to mottled
temp: cool to cold
pain: sharp, numb
Arterial occlusion tx
thrombolytic
embolectomy
Varicose veins
Etiology: gravity, increased abdominal pressure, VALVE INCOMPETENCE
Incidence: Risk factors include prolonged sitting, pregnancy.
pathophysiology: venous pooling leads to distended vein leads to edema and further engorgement.
S/S: primary- appearance; secondary- edema, tired, aching legs
Rx: improve venous return, sclerosis, and ligation
Deep Vein Thrombosis
Etiology: diminished blood flow (especially in the legs) and pressure
RISK FACTORS: prior history of DVT; pregnancy; sitting for long periods; desk job; birth control pills; obesity; smoking
Pathophysiology: hemostasis leads to activation of intrinsic clotting cascade which leads to thrombus formation that is the source of blood clots that break off and travel to different parts of the body *usually to lungs and causing P.E
S/S: tenderness, swelling, redness/ warmth in the affected leg
Rx: anticoagulants (heparin, coumadin, Plavix, Lovenox), and prevention ( what are the modifiable R.F’s)
Peripheral arterial occlusive disease (PAOD)
caused by atherosclerotic blockages in the large arteries like the carotid and femoral. S/s begins to show when an artery is 50% occluded
Main risk factor of PAOD
smoking is the main and hypertension or diabetes might lead to leg amputation.
S/s of peripheral arterial occlusive disease
most common is claudication - which occurs during physical activity and is relieved after a short rest
Pain is caused by the inadequate blood flow due to narrowed and obstructed arteries caused by plaque build-up
thrombangitis
etiology: disease of the arteries and veins in the arms and legs Unknown cause triggered by tobacco use possibly autoimmune
Incidence: YOUNG MEN <35 YEARS OLD WHO ARE HEAVY SMOKERS
Pathophysiology: peripheral arterial inflammation leads to thrombus formation/ vasospasm leads to occlusion
S/s: pain, tenderness, dependent rubor (SHARP)
Rx: SMOKING CESSATION, VASODILATORS, AMPUTATION
Raynaud’s disease/phenomenon/ syndrome
Etiology: Genetics, unknown
Incidence: Young Women
Pathophysiology: TRIGGERS (cold, stress, drugs) leads to digital arterial vasospasm leads to 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 the limb, followed by redness and throbbing pain,
Rx: avoiding triggers vasodilators *(poor circulation in hands so do not put oximeter on fingers)
Coronary artery disease is what
CAD
#1 killer in america
Coronary artery disease
Etiology: *atherosclerosis, vasospasm, thrombi
Incidence: 50% all deaths (35% all deaths in 35-65 yr old)
- Non-modifiable: age > 60, gender especially male, genetic predisposition, type 1 diabetes
-MODIFIABLE: hyperlipidemia (high cholesterol), hypertension, smoking, obesity, sedentary lifestyle, type 2 diabetes
Pathophys: coronary artery occlusion leads to DECREASED MYOCARDIAL PERFUSION leads to myocardial ischemia leads to angina leads to ischemia persists leads to ischemic cells are injured leads to injured cells necrosis leads to myocardium scars over dead tissue leads to DEAD TISSUE WILL NOT CONDUCT ELECTRICAL CURRENT WHICH MEANS NO HEARTBEAT (abnormal EKG readings)
DX tests
EKG, Blood tests, CBC, TROPONIN, ELECTROCYTES, CARDIAC ENZYMES, etc.) Chest x-ray, echocardiogram, angiogram, and cardiac catheterization to open the blocked artery.
Angina Pectoris
CAUSE: TEMPORARY CARDIAC ISCHEMIA CAUSED BY INCREASED MYOCARDIAL WORKLOAD
EKG changes: NONE OR TRANSIENT
Plasma Enzyme levels: Normal
Pain relief: Rest, Nitroglycerin
Beta-blockers, ca++ channel blockers
Infarction (M.I)
cause: irreversible ischemia produces infarction (necrosis or scarring)
EKG changes: PERMANENT abnormal changes
Plasma enzyme levels: ELEVATED TROPONIN AND CK-MB
Pain relief: O2, NITROGLYCERIN, NARCOTICS
ANTICOAGULANTS**, THROMBOLYTICS, ANGIOPLASTY
M.O.N.A
MORPHINE
OXYGEN
NITROGLYCERIN
ASPIRIN
Anticoagulants examples
Aspirin, Heparin, Coumadin, etc.
relationship between troponin and heart attacks
Very high levels of troponin are a sign that a heart attack has occurred.
Cardiomyopathies
Etiology:
- idiopathic dilated cardiomyopathy (IDC), chronic ETOH abuse, infection
- Hypertrophic - genetic predisposition, idiopathic
- restrictive - infiltrative diseases, idiopathic
Pathophysiology: MUSCLE DISEASE LEADS TO ALTERED VENTRICULAR CHAMBER LEADS TO INEFFECTIVE CONTRACTION LEADS TO IMPEDED PERFUSION LEADS TO HEART FAILURE
S/s:
-idiopathic dilated cardiomyopathy (ICD) - fatigue, weakness, palpitations, dysrhythmias, left heart failure
-HYPERTROPHIC - dyspnea, angina, fatigue, syncope, dysrhythmias, left heart failure
-restrictive dyspnea, fatigue, tachydysrhythmias, right heart failure
Rx: SUPPORT AND MAINTAIN FUNCTION, TRANSPLANTATION
Heart failure affects what side of the heart
Right, Left OR both sides
LEFT HEART FAILURE
congestive heart failure
Etiology: MI, hypertension (HTN), aortic valve disease
Pathophysiology of a left-sided heart failure
decreased left ventricular emptying
decreased perfusion to body tissues
increased volume and pressure in the left ventricle
increased volume and pressure in the left atrium
increased volume in pulmonary veins
increased volume in the pulmonary capillary bed
fluid transudate moves from capillaries to alveoli
alveolar space fills with fluid
PULMONARY EDEMA
S/s of left heart failure
exertional and nocturnal dyspnea
hemoptysis (blood-tinged sputum)
orthopnea
cough
cyanosis
elevated pulmonary capillary pressure
DX testing for left heart failure
Chest x-ray
BNP lab test
Remember BNP is excreted from cardiac tissue when the ventricles are stretched
Right-sided heart failure
right-sided heart failure occurs in about 1-20 people, CORONARY ARTERY DISEASE is the most common cause of heart failure
the right ventricle loses its pumping function and blood may back up into other areas of the body
affects the liver, gastrointestinal tract, and the limbs
also may be unable to pump blood to the lungs and left ventricle
Causes of right-sided heart failure
LEFT SIDED HEART FAILURE AND LUNG DISEASE
(chronic bronchitis and emphysema) because the R. ventricle must pump harder to overcome the lung resistance caused by constricted air passages.
Other: heart disease, clots in pulmonary arteries, pulmonary hypertension, and heart valve disease
Symptoms of right-sided heart failure
SWELLING OF THE FEET AND ANKLES
SHORTNESS OF BREATH
DISTENED JUGULAR VEINS
URINATING MORE FREQUENTLY AT NIGHT (NOCTURIA)
Triggers of right-sided heart failure
increased intakes on fluids or salt
fever
infections
anemia
blockages of the coronary arteries
arrhythmias
hyperthyroidism
kidney disease
Pathophysiology of right-sided HF
lower right ventricular emptying
decreases blood supply to the lungs
increases the volume and pressure in R. ventricle causes back up of blood thru-out the system
increased volume and pressure in the great veins
increases volume (size) in distensible organs
increase capillary pressure
leads to peripheral edema and serous effusion
S/s of right-sided heart failure
Fatigue (2ry to low blood O2 perfusion)
distended jugular veins (neck)
enlarged liver and spleen
ascites, GI disturbances
elevated BNP
dependent edema
S/S OF EDEMA
Rx for right-sided heart failure
treat underlying cause; give diuretics to reduce edema and fluid overload; give cardio tonic drugs to improve heart performance
DX testings for right-sided heart failure
CHEST X-RAY, BNP LAB TEST, STANDARD BLOOD TESTS, (CBC, ELECTROLYTES, ETC.)
BNP
BRAIN NATRIURETIC PEPTIDE
Excreted from cardiac tissue
also called B-type Natriuretic peptide
BNP secreted from where
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 where
released into the bloodstream when the muscle tissue of the ventricles is STRETCHED (happens when the heart becomes enlarged like in CHF) the level of BNP in the blood increases when heart failure symptoms worsen and decreases when the heart failure condition is stable.
BNP levels in a person with heart failure
even someone whose condition is stable are 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 in a patient in the urgent care setting in whom the diagnosis is uncertain.
BNP is specific to what
HEART FAILURE
Troponin and CK-MB are specific for what
MYOCARDIAL INFARCTION
Treatment for CHF (left or right sided)
Medication
Lifestyle changes
pacemaker
DX
diagnosis
HX
history of ___
PX
pain
RX
prescription or medications
SX
signs/symptoms
TX
treatment
ABX
antibiotics
2ry
secondary
Effect of morphine
Dilates blood vessels
S/s of compensatory shock
Vasodilation hemorrhage:
Low bp
Lightheadedness
Orhtostatic
Syncope
Adrenergic response
High heart rate and resp rate
Cool clammy skin
Compensation
Narrowing pulse pressure
Lowered mean arterial pressure
Oliguria
Little to no urine output - kidney failure due to hypoxia
Systolic bp cause for concern
Higher than 180 or below 90
Troponin in the blood means what
Cell death in the heart
