MIDTERM ish Flashcards
filler of not known terms after searching quizlet
Is CO2 (carbon dioxide) and acid or a base
Acid; H2O is its counterpart (base)
is NH4 (ammonium) an acid or a base
Acid
is HCO3 (bicarbonate) an acid or a base
Base
is H+ (hydrogen) an acid or a base
Acid
Kidneys regulate secretion and resorption of
H+ (acid) and HCO3 (base)
How does hyperventilating affect CO2 levels
Increases the amount of CO2 exhaled, raising the pH
difference between hyperventilating, hypoventilating, and Kussmaul breaths; and how does each affect CO2 levels?
hypoventilating (slow, shallow breaths): the body produces more CO2 than it can eliminate causing an increase in CO2 in the body, lowering the pH
Kussmaul breaths (fast, deep breaths; a form of hyperventilating): the body is purposely trying to rid the body of excess CO2
normal range of PaCO2
35 to 45 mm Hg
Rise in CO2 = blood O2 decrease
normal range of HCO3
22 to 26 mEq/L
Metabolic Acidosis
(ketoacidosis)
pH: below 7.35
PaCO2: normal (38 to 42 mm Hg)
HCO3: <22 mEq/L $
Increased H+ (hydrogen) / decreased HCO3
Kidneys compensation: retain HCO3, resorption to attempt to raise pH; secretion of H+
Lungs compensation: hyperventilate
Causes: prod./ingestion of acids, renal failure, loss of alkali
Signs: Rapid, deep breaths (Kussmaul); Increased HR; fatigue
Tx: bicarbonate to raise pH;
Respiratory Acidosis
pH: below 7.35
PaCO2: > 45 mmHg $
HCO3: increase 1-3.5 mEq/L for every 10 mmHg CO2 (acute - chronic)
Kidneys compensation: increase production of HCO3; acid in urine
Lungs compensation: Hypoventilate
Signs: Hypoventilation; Abdominal distention, evidence of hypoxia
Tx: treating the underlying illness; use suction to remove mucus from the airway
Metabolic alkalosis
pH: above 7.45
PaCO2: Normal
HCO3: > 26 mEq/L $
Kidneys compensation: excrete HCO3 or conserve H+
Lungs compensation: hyperventilation or hypoventilation
Causes: excess loss of acids, HCO3 retention, ingestion of alkali
Signs: numbness, prolonged muscle spasms, nausea
Tx: treat the underlying condition
Respiratory alkalosis
pH: above 7.45
PaCO2: <35 mmHg $
HCO3: Normal
Kidneys compensation: decreasing production of HCO3 and decreasing acid in urine; acid retention
Lungs compensation:
Signs: hyperventilation; excessive exhalation of CO2
Tx: supplemental O2
Name the chemicals in constant acid-base equilibrium
CO2, H2O, HCO3, H+
edema
clinical manifestation: accumulation of interstitial fluid. Presentation in the extremities is more notable and palpable; however, presentation in the lungs may cause shortness of breath
Tx: typically diuretics are used to aid in elimination of fluid
hyponatremia
Low sodium
Labs: <135 mEq/L
Causes: fluid loss from vomiting and diarrhea or other GI depletion, or an effect from (diuretics); renal dysfunction, adrenal insufficiency (i.e., Addison disease), syndrome of improper ADH secretion, or diabetic ketoacidosis
Signs/symptoms: decreased serum osmolality, headache, anxiety, nausea, hypotension, tachycardia, anorexia, muscle cramps
Tx: focus on underlying etiology, intake/ouput monitoring,
hypernatremia
High sodium
Labs: >145 mEq/L
Causes: increased output or decreased intake of water; excessive intake of sodium, diarrhea, burns, and heat stroke
Signs/symptoms: increased serum osmolality, hypotension, tachycardia, dry skin/mucus membranes, headache, decreased skin turgor
Tx: intake/ouput monitoring, nurse lookout for fever or thirst; increase fluid intake if PT excess water output (diabetes insipidus) - synthetic ADH is warranted … seizure watch
isotonic
solutions have the same osmolality as body fluids.
Normal saline (0.9% sodium chloride) is an example.
hypotonic
the extracellular fluid (ECF) has a lower osmolarity than the fluid inside the cell; water enters the cell
example of a hypertonic solution is 3% sodium chloride.
hypertonic
the extracellular fluid has a higher osmolarity than the fluid inside the cell; water leaves the cell
example of a hypotonic solution is 0.45% sodium chloride.
hypervolemia
Isotonic fluid volume excess typically results from ECF volume excess; increase in ECF sodium
Cause: a decreased excretion of water and sodium, as in acute kidney injury or chronic kidney disease
Clinical manifest: weight gain, decreased hematocrit, dilution of plasma
Signs: distended neck veins, increased BP, and increased capillary hydrostatic pressure contribute to presence of edema.
Tx: restricting fluid intake and correcting the underlying etiology
hypovolemia
Isotonic fluid volume deficit; Normal sodium levels
Causes: hemorrhage, vomiting, diarrhea, fever, excess sweating, burns, diabetes insipidus, and uncontrolled diabetes mellitus
Clinical manifest: decrease in urine output, weight loss, and an increased hematocrit.
Signs: tachycardia, decreased skin turgor and blood pressure, and, potentially, hypovolemic shock
Tx: addressing the cause of the fluid deficit and replacing lost volume
RAAS
renin-angiotensin-aldosterone-system
responds to low blood pressure and low serum sodium
Ex:
decrease in BP will stimulate the secretion of renin and subsequent activation of RAAS, resulting in sodium retention, increased fluid volume and BP increase
renin
controls production of aldosterone
aldosterone
mineralcorticoid hormone synthesized and secreted by adrenal cortex, in response to hemodynamic changes
helps control the balance of water and salts in the kidney by retaining sodium in and releasing potassium from the body
decreased/increased serum osmolality
low serum osmolality will suppress the release of ADH, resulting in decreased water reabsorption and more concentrated plasma
increase of only 2% to 3% in plasma osmolality will produce a strong desire for thirst
hyperchloremia
High chloride ions
Labs:
Causes:
Signs/symptoms:
Tx:
obstructive shock
caused by an obstruction of blood flow
least common for nurse to encounter in ICU
cariogenic shock
failure of hear to pump
distributive shock
abnormal redistribution of blood
types: anaphylactic, septic, neurogenic
hypovolemic shock
low blood volume
septic shock
(or anaphylatic shock) due to inflammatory vascular response
a type of distributive shock = most common in ICU
sepsis (general)
the bodys extreme response to infection; can lead to tissue damage, organ failure, and death
all shock types (etiology)
development of acute circulatory failure resulting in hypotension and inadequate tissue perfusion; heart failure, low blood volume, redistribution of ECF to extravascular sites, and obstruction of blood flow
OUTCOME: poor tissue perfusion
perfusion
flow rate of blood through capillaries and extracellular spaces, responsible for transport of O2, nutrients, and waste
hypoperfusion (clinical manifestation)
cold, clammy skin (a result of vasoconstriction and cyanosis), renal output decrease (oliguria), confusion (obtundation), hyperlactatemia, and hypercoagulability
oliguria
production of abnormally small amount of urine
hypovolemic shock (cause)
loss of >15% of body fluid
severe dehydration, inadequate ECF, sig. blood loss, excess vomit/diarrhea, MODS, burn injury
cardiogenic shock (s/s)
decreased CO (cardiac output), MI, HF, cardiac tamponade, restrictive cardiomyopathy, constrictive pericarditis, MODS
obstructive shock (s/s)
clinical : disturbance of consciousness, oliguria, hypotension, and tachycardia
obstruction of major blood vessels, obstruction of cardiac pumping, cardiac tamponade, pulmonary embolism, MODS
distributive shock (s/s)
clinical :
imparied distribution of blood flow, extensive vasodilation, loss of vascular tone, septic shock, anaphylactic shock, neurogenic shock, MODS
sepsis (s/s)
hemodynamics (factors that influence circulation)
blood volume, systemic vascular tone, heart rate, force of contraction
MODS
multi-organ dysfunction syndrome
stage 1 shock
early, reversible, compensated
sympathetic activation cause tachycardia and vasoconstriction
kidneys respond with active RAAS to reabsorb sodium and water to maintain fluid
strong chance of recovery
stage 2 shock
intermaediate, progressive
compensation begins to fail, decrease in persuion = hypoxia
PT experience confusion, disorientation, angina (d/t decreased O2 delivery to myocardium), muscle pain
reversible if right treatment is implemented promptly
stage 3 shock
refractory, irreversible
permanent toll on body and organs
heart func. decline, kidneys shutdown, cells = hypoxia and cell death
PT death due to MODS
qSOFA
(Quick Sequential Organ Failure Assessment)
bedside diagnosis criteria for septic shock
(altered mentation) Glasgow coma scale <10, systolic BP of 100mmHg or less, and respiratory rate of 22/min +
Neurogenic shock
blockage of sympathetic nervous system outflow to the intrathoracic sympathetic chain
caused by any factor that increases parasympathetic stim
common in spinal cord injury above T6, 2nd to parasym. outflow from T1-L2
more severe = higher on spinal cord
neurogenic shock (s/s)
decrease in vascular resistance, loss of vascular capacitance with assoc. vascular dilation and bradycardia in the absence of hypovolemia
hypovolemia = tachycardia
Clinical : systolic hypotension, bradycardia, hypothermia
SOFA
evaluates multiple different systems (cardiovascular, respiratory, coagulation, renal, hepatic, neurologic)
predicting potential mortality and can guide clinical intervention
anaphylactic shock (s/s)
stridor, tachycardia, dyspnea, wheezing, coughing, edema, laryngospasm, bronchoconstriction, angioedema, urticaria, pruritus, hives, gastrointestinal cramps, and hypotension
MODS
multi-organ dysfunction syndrome
2+ system dysfunction; homeostasis in PT cannot be maintained without intervention
most commonly caused by septic shock
MODS (s/s)
6 primaries (respiratory, renal, hepatic, cardio, gastro, neuro)
Renal & hepatic = serum creatinine or bilirubin levels. Hematologic = thrombocytopenia
Cardio = changes in blood pressure and the heart
Neuro = level of consciousness
Gastro = tenderness of abdomin, palpable masses
Assessment will focus on Glasgow Coma scale scores
ischemia
drop in bloodflow to the brain; a lack of O2 and glucose that lead to tissue dmg
hematoma
increasing pressure in the skull (bleeding in tissue or excess prod. of CSF)
CSF
(cerebral spinal fluid)
choroid plexi produces CSF within ventricles
flows in the subarachnoid space surrounding the brain and spinal cord, providing buoyancy and nourishment
hydrocephalus
excessive accumulation of CSF in brain can cause increased pressure within skull
BBB
(blood brain barrier)
specialized endothelium in brain capillaries that permits selective entry of substances
Highly lipophilic subs are able to cross, H2O by diffusion and most others by facilitated diffusion
cerebral autoregulation
critical to providing a steady flow of O2 and nutrients to brain and removing metabolic waste; maintains blood flow to brain and spinal cord despite fluctuation in mean arterial pressure
cerebral blood flow
blood supply to the brain in a given time
intracranial pressure
pressure exerted by contents of cranium: brain tissue, blood, and CSF
TIA
(transient ischemic attack)
temporary episode of neurologic dysfunction cause by focal brain, spinal cord, or retinal ischemia without acute infarction
cause : clot that blocks bld supply to brain; does not cause permanent damage
buildup of fatty deposits on arterial walls (atherosclerosis)
TIA (s/s)
facial drooping, extremity weakness (esp. one sided), speech difficulty, sudden trouble seeing, difficulty walking with dizzy, lack of balance, severe headache unkown cause
TIA (Tx)
(w/in 24-48hrs) urgent evaluation, risk stratification, and PT education of stroke prevention therapy
TIA mimics
hypoglycemia, seizure, intracranial hemorrhage
stroke
interruption in bld supply to brain or bleeding vessel that results in brain tissue dmg or infarction
ischemic stroke
partial or complete occlusion od cerebral bld flow to an area of the brain d/t a thrombus or embolus
athersclerosis = most common lead
(conditions = increased risks pg. 672)
thrombotic stroke
occlusion of bld vessel as a result of plaque buildup along vessel wall, usually involve internal carotid, mid-cerebral, or basilar artery
hemorrhagic stroke
bleeding in brain d/t bursted bld vessel
(intraparenchymal) intracerebral = bld in brain tissue (parenchyma)
intraventricular = bld in ventricles
extracerebral = bld in membrane surrounding brain
aneurysm
abnormal bulge along vessel wall that fills with bld and is caused by a weak or thin area of wall
symptoms occur when it puts pressure on brain or it leaks/ruptures causing a hemorrhage
AVM
(arteriovenous malformation)
tangle of abnormal/poorly formed bld vessels
can occur anywhere and are at the greatest risk of bleeding
Dural AVM = acquired disorder (usually trauma)
AVM (s/s)
(would be considered a stroke)
sudden onset of neurologic deficit that lasts 24hr and is due to a reduction or occlusion of cerebral circulation or rupture of blood vessels
s/s : fig. 27.3
ischemic stroke (Tx)
restore bld flow and reduce area of infarction (brain tissue death); area surrounding the infarction (penumbra) can be salvaged if perfusion is restored quickly
Acute stroke : O2 is used to improve oxygenation, glycemic control to norm rng, and BP managed for adequate perfusion
DCI
(delayed cerebral ischemia)
neurologic deficit, cognitive deficit, or both that occur in 3-14 days after hemorrhage
hemorrhagic stroke Tx
priority of care = ventilation and BP management
osmotic dieuretics = decreased intrcranial pressure
subdural hemorrhage
bleed from the bridging veins below inner layer of dura (between dura mater and arachnoid membrane)
does not directly occlude bld vessels, so is not considered a stroke; can become large enough to cause a stroke though
subdural hemorrhage (s/s)
headache, confusion, behavior change, dizziness, nausea, vomiting, lethargy, weakness, apathy, seizures
size of hemorrhage and age of PT affect response
subdural hemorrhage (Tx)
surgery must be considered
before surgery, ventilation and BP are priority
spinal cord hemorrhage
rare but may occur with trauma, vascular malformation, or bleeding disorders
(epidural, subdural, subarachnoid, or intramedullary)
intramedullary = bleed in white + gray matter
epidural/subdural = compression on spinal cord
spinal cord hemorrhage (s/s)
sudden, severe, localized back pain with or without radiculopathy
intramedullary = hemiparesis, paraparesis, or quadriparesis; sensory loss below the lesion; and loss of sphincter control
hemiparesis
weakness or inability to move one side of body
paraparesis
partially unable to move legs
quadriparesis
(tetraparesis) muscle weakness in all four limbs
tetraplegia
inability to move upper and lower body
spinal cord hemorrhage (Tx)
surgical resection for decompression or catheter-based intervention, raditation therapy (photon or gamma knife)
HF
(heart failure)
inability of heart to pump adequate bld to meet bodys metabolic needs
HF (causes)
muscular contraction = decreased ejection
muscular relaxation = heart not filling adequately
combo
HF (s/s)
fatigue, SOB, inability to exercise, extremity edema, death
CO
(cardiac output)
amount of bld pumped out of heart in L/min
RAAS (response to CO)
if CO decreases = RAAS & SNS are activated
fluid retention and vasoconstriction
left side HF
left = responsible systemic circulation; failure results in vol. overload & venous congestion in lungs
s/s : fatigue and SOB;
decreased CO = RAAS & SNS active = bld volume increase = pulmonary congestion = dyspnea
pulmonary congestion = right side works harder against the pressure and may fail as a result
right side HF
right = responsible lungs circulation; failure results in systemic venous congestion = elevated jugular ven. pressure, hepatic congestion, peripheral edema
everything behind the failure gets backed up
systolic failure
HF with reduced EF
amount of bld present at end of diastole (preload) is important
diastolic failure
EF is preserved, contractility is preserved or slightly impaired, but muscle relaxtion impaired = inadequte filling, decreased preload = reduced CO
impaired fill (bigger issue) = tachycardia + diastolic fill time decreased = even more reduced SV
SV
(stroke volume)
amount of blood pumped out of heart with each beat in mL
EF
(ejection fraction)
measurement of percentage of blood ejected from left ventricle with each contraction
High output HF
heart still pumping high amount of blood (8L/min);
vasodilation + BP decrease
Low output HF
(simply HF)
CO reduced = decreased perfusion
acute HF
isolated event without prior hx
rapid prog. to critical illness; MI, myocarditis, drug toxicity
PT may suffer chronic HF after
Tx : underlyting cause
chronic HF
management : low-salt diet, medications, monitor symptoms/vitals, lifestyle decisions
(ADHF; acute decompensted HF) chronic HF PT can still develop acute HF = worsening symptoms
any stress to the heart can result in decomp. (inf./diet/lifestyle/meds)
Tx : hospital and underlying cause to be idetnified and treated
NYHA Class 1
does not affect daily activity
NYHA Class 2
comfortable resting, but slight limit in activity
NYHA Class 3
markedly limited in physical activity, still comfort at rest
NYHA Class 4
experience symptoms at any level of activity and sometimes at rest
ACC/AHA Stages of HF
Stage A: high risk for HF w/o structural dis or symptoms
Stage B: structural dis but w/o s/s of HF
Stage C: structural dis w/ prior or current symptoms
Stage D: refractory HF requiring specialized interventions
Killip Classification
Class I: No heart failure. No clinical signs of cardiac decompensation
Class II: Heart failure. Diagnostic criteria include rales, S3 gallop and venous hypertension
Class III: Severe heart failure. Frank pulmonary edema
Class IV: Cardiogenic shock. Signs include hypotension (systolic blood pressure of ≤90 mmHg) and evidence of peripheral vasoconstriction such as oliguria, cyanosis, and diaphoresis. Heart failure, often with pulmonary edema, has been present in a majority of these patients.
systolic HF (cause)
dilated cardiomyopathy (weakening of heart muscle) idiopathic, ischemic (related to Coronary Artery Disease), or genetic
CAD w/ MI, diabetes, thyroid, hormonal
alcohol or cocaine
nutritional deficiencies, chemo
Preload
amount of blood in the ventricle before contraction, at the end of diastole
affected by: body fluid volume, venous return to heart, and EF (ejection fraction)
Afterload
amount of pressure the heart needs to generate to pump blood out of the ventricle
the ventricle must contract strongly enough to overcome the blood pressure in that system
Reducing afterload typically allows the heart to work more efficiently
contractility
strength of muscular contraction in the heart muscle. Greater contractility typically leads to increasing stroke volume
SVR
(systemic vascular resistance)
resistance to forward flow of blood generated by the blood vessels in the systemic circulation
Normal SVR is 800-1200 dynes-sec/cm^5.
Low SVR = lower pressure needed to provide fwd flow
blood flow through the heart
right atrium > tricuspid > right ventricle > pulmonary valve > lungs > left atrium > mitral > left ventricle > aortic
cardiac remodeling
physical hypertrophy of heart muscle, becomes less coordinated with opposing ventricles, less elongated fibers, shorter and more rounded
Angiotensin II contributes to promoted hypertrophy
systolic HF (s/s)
fatigue, sleep disturbances, weight loss, anorexia, and dyspnea
depression and cognitive dysfunction is also common
peripheral edema, diminished distal pulses, hypotension, tachycardia, and narrow pulse pres-sure
pulmonary edema and hepatic congestion may also develop, manifesting in cough, frothy sputum, and right upper quadrant tenderness or pain.
systolic HF (Tx)
reducing symptoms by decreasing fluid retention and counteracting the neurohormonal effects of HF. ACE inhibitors are considered first-line therapy in the treatment of systolic HF.
diastolic HF (cause)
stiffnes of hear muscles, abnormal electrolyte movement into and out of the myocardial cells causing failure of the heart muscle to completely relax
diastolic HF (s/s)
dyspnea with exercise, more fluid retention in abdomin (PT describe as bloating or fullness)
diastolic HF (Tx)
No therapy has been shown to improve survival in patients
treat PT according to underlying disease
left-side HF (cause)
cardiomyopathy, coronary artery disease, alcohol or cocaine abuse, or hypertension
left side HF (s/s)
hypertrpophic heart, increase in pulmonary venous pressure = paroxysmal nocturnal dyspnea, activation of RAAS = increase in preload and afterload
reduced CO = hypotension, fatigue, decreased urine output, exercise intolerance, dizziness, syncope, distal pulse decrease, cool skin, tachycardia, BP low, weight loss
paroxysmal nocturnal dyspnea
sudden shortness of breath while sleeping
orthopnea
difficulty breathing while laying flat
left-side HF (Tx)
similar to systolic HF: reversing the effects of the body’s natural responses to the HF, Fluid retention is alleviated by the use of diuretics, RAAS is blocked by the use of ACE inhibitors
PT educated to weigh themselves, monitor vitals, and low-sodium diet
right-side HF (cause)
typically caused by left-side HF
pulmonary HTN (pressure too great for afterlod of right ventricle to pump), ischemia, contractility reduction
right-side (s/s)
In right ventricular failure, the left ventricle is inadequately filled, leading to reduced CO.
Patients may exhibit s/s of reduced CO, including cool extremities, poor distal pulses, fatigue, exercise intoler-ance, and syncope
Patients may complain of nausea, vomiting, and early satiety as the liver enlarges and causes pressure on the stomach, liver function may be impaired
elevated jugular venous pressure, distended neck veins, peripheral edema
pulmonary vascular resistance
the resistance to flow of blood generated by the blood vessels in the pulmonary circulation
right-side HF (Tx)
dependent on underlying cause; help reduce RV afterload and improve RV failure; low sodium diet
high output HF (cause)
marked by unusually low SVR and elevated CO; caused by dilation of vascular bed or arteriovenous fistula
decrease SVR = anemia (nitric oxide > vasodilation), sepsis
arteriovenous fistula
abnormal connection between 1+ arteries and 1+ veins = systemic shunting
(caused by): Paget disease, multiple myeloma, liver disease, or an artificially created fistula such as one created for dialysis
high output HF (s/s)
similar to systolic, (and right side HF) signs of volume overload such as hepatic congestion, elevated jugular venous pressure, and peripheral edema. Patients may also experience fatigue and dyspnea
high output HF (Tx)
treating cause of vasodilation, control symptoms, and support vital functions
cardiac index
value obtained when the CO is divided by body surface area
CAD
(coronary artery disease)
bloodflow to myocardium is reduced
sometimes interchangeable w/
(coronary heart disease)
buildup of plaque (made of cholesterol) [fatty] deposits in the coronary arteries (atherosclerosis)
Dx included with CHD: silent myocardial ischemia, myocardial infarction, angine pectoris, acute coronary syndrome (ACS)
angina
(angine pectoris)
chest pain, discomfort, pressure, squeezing symptoms of CAD when the heart is not receiving enouhg perfusion blood
CVD
(cardiovascular disease)
commonly atherosclerosis, causes disease of the heart and coronary and systemic circulation
Dx include: stroke, TIA, claudication, and limb ischemia
claudication
leg pain that is induced by exercise, typically caused by decreased arterial blood flow
myocardial ischemia
restriction or decrease in bld supply to the heart muscle tissues = shortage of O2
myocardial infarction
complete occlusion of bld flow leading to cell death, or necrosis
athersclerosis > thromboembolism
thrombus (blood clot) is carried through the vessel and becomes lodged (embolism)
ideal cardiovascular health
w/o cardiovascular disease
Life Simple 7: BP, physical activity, cholesterol, diet, weight, smoking habits, blood glucose
thrombosis
process of formation of a thrombus that obstructs blood flow to organs depending on where it comes from; when formed in coronary artery, the block can cause an MI
vasospasm
a sudden contstriction of a blood vessel that decreases the vessels diameter and thus decreases blood flow
aneurysm
a localized, blood-filled, balloon-like bulge in the wall of a blood vessel
a name for atherosclerosis that can affect all arteries in the body?
ASCVD (atherosclerotic cardiovascular disease)
dysrhythmia
abnormal heart rhythm that can be irregularly slow or fast (aka arrhythmia)
coronary angiography
(aka coronary arteriography)
invasive procedure that is usually used to confirm the diagnosis of CAD after noninvasive test have been inconclusive
coronary perfusion pressure
the pressure of blood through coronary circulation as a result of the pressure gradient between the aortic pressure and the right atrial pressure
autoregulation
the phenomenon that maintains the constant regulation of coronary blood flow through the myocardium despite changes in coronary perfusion pressure
tachycardia
(abnormal rapid heart rate, generally more than 100 beats per minute)
stable angina
occurs with increased myocardial oxygen demand and reduced blood flow during exertion or emotional stress, commonly caused by atherosclerosis
stable angina (cause)
gradual narrowing of the arteries: endothelial dysfunction, coronary microvascular disease (MVD), vasospasms
stable angina (s/s)
chest discomfort {usual complaint}, may also result as postpandrial (after eating), dyspnea, fatigue, belching
same as angina pectoris, sqeezing, tightness, crushing, suffocating, and pressure
stable angina (Tx)
stress test (cardio-vascular magnetic resonance (CMR) myocardial perfusion imaging)
Beta blockers, ACE inhibitors, or ARBs when ACE are not tolerated
short-acting nitroglycerin
silent ischemia
higher prevalence being likely for patients with diabetes
silent ischemia (cause)
thought to be due to defective anginal warning as a result of an issue with peripheral and neural processing of pain
silent ischemia (s/s)
chest pain may not always be present; ST-segment depression may or may not be present
IHD
ischemic heart disease
silent ischemia (Tx)
tx of symptomatic and asymptomatic ischemia would be similar = nitrates, beta blockers, CCBs (reduce or eliminate episodes)
lipid-lowering therapy as secindary
MVD (cause)
not currently known, could be d/t ischemic process or other causes such as endothelial and microvascular dysfunction, coronary vaso-spasms, or myocardial metabolism problems
MVD
(microvascular dysfunction or coronary microvascular dysfunction)
damage to the walls and inner linings of small coronary arteries that can lead to narrowing, spasms, and decreased blood flow
MVD (s/s)
angina in the absence of ischemia caused by CAD is a common characteristic, difficult to differentiate from angina with ischemia
MVD (Tx)
standard test used to detect CAD do not work for MVD;
noninvasive methods: Doppler echocardiography, SPECT scan, and CMR myocardial perfusion imaging, have proved helpful in detecting MVD
ACS
(acute coronary syndrome)
acute form of CAD; any cluster of clinical signs and symptoms that are related to acute myocardial ischemia and infarction
Types:
- non–ST-segment elevation acute coronary syndrome (NSTE-ACS), which formerly was known as unstable angina
- non–ST-segment elevation myocardial infarction (NSTEMI)
- ST-segment elevation myocardial infarction (STEMI)
NSTE-ACS
(non–ST-segment elevation acute coronary syndrome)
formerly known as unstable angina
presents as myocardial ischemia without ST elev.
accelerates in frequency and severity but does not result in myocardial necrosis
{ischemic}
NSTEMI
(non-ST-segment elevation mycardial infarction)
myocardial ischemia in the absence of ST elevation on ECG but the presence of elevated biomarkers of myocardial necrosis = acute MI
major difference between NSTEMI and unstable angina is the biomarker of necrosis
{infarction}
STEMI
(ST-segment elevation mycardial infarction)
myocardial necrosis
more precise term for heart attack
{infarction}
unstable angina
chest discomfort or pain related to lack of blood flow through coronary arteries and subsequent myocardial ischemia that is less predictable than stable angina and may occur at rest
STEMI (cause)
state of heightened inflammation and prothrombotic components
adv. atherosclerosis, nonobstructive plaque rupture, embolus
exposure to fine particle pollution could increase risk of ACS,
atrial fibrillation
dys-rhythmia that may cause pooling and clotting of blood and the risk of embolization if the clot breaks free and obstructs an artery
STEMI (s/s)
ischemic nerve endings cause pain, but necrotic myocardium will not
angina, dyspnea, malaise (radiate to shoulder, arms neck), fatigue, diaphoresis, palpitations
bradycardia
less than 60BPM
STEMI (s/s)
ischemic nerve endings cause pain, but necrotic myocardium will not
angina, dyspnea, malaise (radiate to shoulder, arms neck), fatigue, diaphoresis, palpitations
STEMI (Tx)
ECG alone is not sufficient to Dx a STEMI
timely reperfusion and function of caridomyocytes
Timely Percutaneous coronary intervention (PCI), also known as coronary angioplasty, is a nonsurgical technique for treating obstructive coronary artery disease, including unstable angina, acute myocardial infarction (MI), and multivessel coronary artery disease (CAD) will greatly increase survival chance.
automaticity
ability of specialized myocardial cells, or pacemaker cells, to generate an electrical impulse (depo-larize) to regulate the heart rate in accordance to the body’s needs.
absolute refractory period
time after the firing of a nerve fiber during which the nerve fiber can-not be stimulated, regardless of the strength of the stimulus applied
VF
(ventricular fibrillation)
most serious dysrhythmia; has greatest risk of occurence within first hour of MI
related to absolute refractory period
which electrolyte imbalances have the greatest risk for heart dysrhythmias?
hypokalemia and/or hypomagnesemia
ventricular aneurysm
defect in the left or sometimes right ventricle wall in which there is bulging outward dur-ing both systole and diastole, usually as a result of a MI
(cause) female, LAD artery occlusion, no Hx of angina
(s/s) 3-4 heart sound present, systolic murmur
TTE (transthoracic echocardiography) used to identify
ventricular septal rupture
type of ventricular septal defect in which there is an abnormal opening between the left and right ventricles causing oxygenated blood (from the left ventricle) to mix with deoxygenated blood (from the right ventricle) as a result of left-to-right shunting.
pericarditis
swelling and inflammation of the pericar-dium, the thin double-layered sac surrounding the heart, as a result of injury such as an acute MI, infection, inflam-matory disorder, trauma, cancer, or congenital causes
10% chance to accour 23-96hrs post-MI
Dressler syndrome
also known as post-MI syndrome, is the late pericarditis and possibly has an autoimmune pathogenesis
pericarditis (s/s)
pleuritic chest pain, pain worsens with deep inspiration, cough, swallow, lying down
pericardial friction may rub and be auscultated
pericarditis (Tx)
hospitalization for management and OBS of possible cardiac tamponade, aspirin every 4-6hr to reduce inflammation and treat pain
cardiac tamponade
life-threatening condition of increased pericardial pressure as a result of blood or fluid buildup between the myocardium and the pericardium
cardiac tamponade (cause)
pericardial effusion (fluid accumulation), trauma, inf, cancer, med side effect, HF, MI, raditation, Dressler, PCI, surgery, inflammatory disease
cardiac tamponade (s/s)
dyspnea, edema, oliguria (low urine output), jugular venous distention, tachypnea {pant}, and tachycardia
cardiac tamponade (Tx)
prompt surgical Tx is needed, MRI can confirm presence, fluid removed and examined to identify cause
valvular disorders
problems that disrupt blood flow through the atria and ventricles as a result of abnormal func-tioning of one or more of the four heart valves such as stenosis, regurgitation, or prolapse
the four heart valves?
atriventricular: tricuspid and mitral
semilunar: pulmonic and aortic
valvular disorders (cause)
Increased risk of valvular disorders is associated with age, gender, tobacco use, high cholesterol levels, hypertension, and diabetes
regurgitation
leaking valve; not closing completely
prolapse
valves don’t close smoothly, or overextend into next chamber (balloon)
stenosis
hardening or fusion; in the case of mitral valve, may be fused together and restrict blood flow; or could be hardened in an open state and function improperly
valve disorder (Tx)
surgical replacement
coronary collateral circulation
can develop in the heart as an adaptation to ischemia; as an alternative path for blood supply
PVD
(peripheral vascular disease)
general term referring to conditions affecting circulation in the tissues other than the brain or heart
affects veins; chronic venous insuffi-ciency, deep vein thrombosis, leg ulcers, and varicose veins
PAD
(peripheral artery disease)
affects arteries, caused by arteriosclerosis
arteriosclerosis
thickening, loss of elasticity, clacification of walls of arteries
atherosclerosis
build up of plaque within artery that harden and narrow
plaque is made of
cholesterol, calcium
hyperlipidemia
(form of dyslipidemia)
elevated level of blood lipids
LDL
(Low-density lipoproteins)
primary carriers of cholesterol
“Less-Desireable Lipoproteins”
HDL
(high-density lipoproteins)
help to clear cholesterol from the arteries
“highly-desireable lipoproteins”
atheroma
region of plaque consists of calcium, macrophages, lipids, and fibrous connective tissue, where atherosclerotic narrowing begins to build up
vulnerable plaque
more inflammation and thinner fibrous cap, more susceptible to rupture with subsequent thrombi formation
arterial dissection
caused by a tear in the tunica intima in which the blood vessel splits and blood goes between the inner and outer layers, separating the walls
trauma, heredity, cocaine use, pregnancy, and hyperten-sion are associated risk factors
angioplasty
stent placement is the minimally invasive procedure
A balloon-tipped catheter is placed into an artery and advanced to the area of blockage. The balloon is inflated, pressing the plaque against the arterial wall. Once opened, the balloon is deflated, and a small wire mesh tube called a stent is placed in the vessel to keep it from narrow-ing or closing again
NAPAD
(Nonatherosclerotic peripheral arterial disease)
group of disorders in which blood flow is decreased for reasons other than plaque buildup
coarctation of the aorta, thoracic outlet syndrome, and Raynaud disease
TOS
(thoracic outlet syndrome)
thoracic outlet starts at the base of the neck and goes behind the clavicle, over the first rib, and down the arm
If the path is narrowed, it can restrict the flow of blood and nerve function
(s/s) poor bld flow or decreased nerve function
coarctation
birth defect resulting in narrowing of aorta
Raynaud disease
condition characterized by attacks of vasospasm in the small arteries and arterioles in the fingers
often triggered by cold weather and emotional stress
Primary (idiopathic), secondary (caused by another condition)
(s/s) skin devoid of color, cyanotic, numbness, tingling, ischemia may result in ulceration or necrosis
Raynaud (Tx)
events may not be severe enough for medical attn.
tx for 2nd addresses underlying condition
prime med is calcium channel blockers
CVI
(chronic venous insufficiency)
disorder in which the veins are unable to return adequate blood to the heart
long-term disorder that most com-monly occurs as a result of blood clots in the deep veins of the legs, a condition called deep vein thrombosis (DVT)
CVI (causes)
genetic predisposition, gender (the disorder is more com-mon in women), pregnancy, age over 50 years, smoking, lack of physical activity, obesity, and occupations requiring long periods of standing or sitting. Use of oral contracep-tives
CVI (s/s)
leg cramps and pain that worsens when standing, edema of leg, thickening or discoloration of skin on calves
leg ulcers
(CVI is most common cause)
sores on the skin that persist for more than 6 weeks and take several months or longer to heal
varicose veins
veins that have become enlarged and twisted because of the rupture of valves
superficial thrombophlebitis = inflam of varicose veins
DVT
(deep vein thrombosis)
a thrombus (blood clot) occurs in a vein deep in the body; the thrombus may become an embolism that can travel to the heart, lungs, brain, or other vital organs of the body.
(s/s) pressure builds, fluid starts to leak out of the swollen veins, causing edema and additional pain. The area may become reddened, hard, and warm as a result of blood backing up in the area.
DVT (Tx)
a positive D-Dimer indicates high amount of fibrin degradation and suggests clot formation
Obesity is the main culprit for DVT
Elevated BP
120-129 AND < 80
Stage 1 HTN
130-139 OR 80-89
Stage 2 HTN
> 140 OR >90
Stage 3 HTN
> 190 AND/OR >120
essential HTN
(primary HTN)
HTN that does not have a known cause
90% of the cases
secondary HTN
identifiable and categorized cause
hypertensive urgency
patient presents with severe HTN without evidence of organ damage
hypertensive crisis (s/s)
myocardial ischemia or infarction. Renal function is diminished, and blood or protein may be found in the urine. Acute renal failure may occur. In the brain, thrombotic or hemorrhagic stroke may occur. The capillaries in the brain become leaky, producing hypertensive encephalopathy (edema of the brain), with symptoms of headache, paralysis, seizures, or coma. Reti-nal hemorrhages and edema of the retina (papilledema) are signs of severe HTN.
hypertensive crisis
rare condition that occurs when systolic pressure exceeds 180 and/or diastolic pressure exceeds 120 mmHg.
formerly called malignant hypertension or hypertensive emergency
Organ damage occurs primarily in the cardiovascular system, kidneys, or brain
