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CARDIAC DISORDERS-PATHOPHYSIOLOGY-EXAM 2

Terms in this set (177)

_____ _______ changes in the normal function in response to smoking, hyperlipidemia, diabetes and obesity-RISK FACTORS?
ENDOTHELIAL DYSFUNCTION
______ FATS, CHOLESTEROL, TRIGLYCERIDES?
LIPIDS
______ Carriers of lipids in the blood?

EX: HDL, LDL,-MAIN
LIPOPROTEINS
What are the five types of lipids?
Chylomicrons, VLDL, IDL, HDL, LDL
FUNCTION OF THE _________?

-SELECTIVELY PERMEABLE BARRIER
-Modulates blood flow and vascular reactivity
-Regulates thromobosis
-Regulates cell growth
-Regulates inflammatory/immune response
-Maintains extracellular matrix
-Involved in the metabolism of liproteins
ENDOTHELIUM
_______ attach to receptors on cells in the tissues transfer of triglycerides and cholesterol?
APOLIPOPROTEIN
______ NONEXCHANGEABLE, remain attached to the same lipoprotein particle from biosynthesis to breakdown.
B 100 (LDL, VLDL)
_______ EXCHANGEABLE, are able to dissociate from one lipoprotein and associate with another.
A1, A2, A4. (HDL)
______ moving from the Intestines to the tissues to the liver?
EXOGENOUS
______ moving from the liver to the tissues and back?
ENDOGENOUS
______ are absorbed from diet in the intestine as chylomicrons?
LIPIDS
______ carries absorbed cholesterol & triglycerides?
CHYLOMICRONS
Adipose and muscle cells take up lipids from chylomicrons-remnants are ______ ?
IDLs
IDLs become ______?
LDLs
______ delivers cholesterol to the liver and other tissues?
LDL
________ carries cholesterol back to the liver from the tissues?
HDL
________ carries triglycerides?
VLDL
______,______,______, into the blood? (ENDOGENOUS)
LDL, HDL, VLDL
______ BAD CHOLESTEROL-delivers cholesterol to the tissues?
LDL
_______ GOOD CHOLESTEROL-protects against ATHEROSCLEROSIS-taking cholesterol from the tissues and moving it back?
HDL
_______ triglyceride (MAJOR CORE LIPID), B-100, E, OTHERS, (APOLIPOPROTEIN) delivers triglycerides to non-hepatic tissues PROBABLE CONTRIBUTOR to ATHEROSCLEROSIS?
VLDL
______ cholesterol (MAJOR CORE LIPID), B-100,(APOLIPOPROTEIN),
delivers cholesterol to non-hepatic tissues DEFINITE CONTRIBUTOR to ATHERSCLEROSIS?
LDL
_______ cholesterol (MAJOR CORE LIPID), A-1, -2, A-IV, (APOLIPOPROTEIN), transports cholesterol from non-hepatic tissues back to liver PROTECTS AGAINST ATHERSCLEROSIS?
HDL
Elevation of ______ cholesterol INCREASES risk of CHD ( Coronary Heart Disease)?
LDL
Elevation of _______ cholesterol REDUCES risk of CHD (Coronary Heart Disease?
HDL
______ are responsible for promoting the removal of LDL cholesterol?
RECEPTORS
HYPERCHOLESTEROLEMIA- ____________
CHOLESTEROL DEPOSITS?
XANTHOMAS
(OPTIMAL) LDL level is LESS < than ____?
100
(DESIRABLE) TOTAL CHOLESTEROL level is LESS < than _____?
200
(HIGH) HDL CHOLESTEROL level is > GREATER than _____?
60
(LOW) HDL CHOLESTEROL level is LESS than ______?
40
________ paste or gruel hardening
accumulation of fatty material in an artery wall, leading cause of CAD (CORONARY ARTERY DISEASE), PAD (PERIPHERAL ARTERY DISEASE) and STROKE, progressive disease with age _________?

COMMON SITES:

1. ABDOMINAL AORTA and ILIAC ARTERIES
2. PROXIMAL CORONARY ARTERIES
3. THORACIC AORTA, FEMORAL and POPLITEAL ARTERIES.
4. INTERNAL CAROTID ARTERIES
5. VERTEBRAL, BASILAR, and MIDDLE CEREBRAL ARTERIES.

RISK FACTORS:

CIGARETTE SMOKING
OBESITY
HYPERTENSION
HYPERLIPEDEMIA with elevated low-density lipoprotein and low high-density lipoprotein cholesterol.
DIABETES MELLITUS

MALE GENDER
GENETIC DISORDERS of lipid metabolism
FAMILY HISTORY of PREMATURE CORONARY ARTERY DISEASE.
ATHERSCLEROSIS
Common site of ATHERSCLEROSIS?
ABDOMINAL AORTA and ILIAC ARTERIES
________ disjunction starts the disease process of ATHERSCLEROSIS?
ENDOTHELIAL
_________ accumulates over your lifetime, NOT AN ACUTE DISEASE?
ATHERSCLEROSIS
ATHERSCLEROSIS consist of three lesions ______, ______, _____?
FATTY STREAKS, FIBROUS PLAGUES, COMPLICATED LESIONS
The development of atherosclerotic lesions is a progressive process involving _______, ________, __________?
1. Endothelial cell injury and inflammatory cells migrate.

2. Foam cell formation and lipid deposits

3. Plague with a lipid core
ARTERIAL DISORDERS 0F ____________?

CLINICAL MANIFESTATIONS:

-Usually none until severe narrowing, blocking of the artery.

COMPLICATIONS:

-Rupture, thrombus formation-Ischemia, injury, infarction of cells.

-ANEURYSM
Atherosclerosis
What are the RISK FACTORS for endothelial dysfunction?
SMOKING, HYPERLIPIDEMIA, DIABETES and OBESITY
What are the five types of LIPOPROTEINS?
CHYLOMICRONS, VLDL, IDL, HDL, LDL
Which lipoprotein primarily carries CHOLESTEROL?
LDL
Which lipoprotein primarily carries TRIGLYDERIDES?
VLDL
Which lipoprotein CARRIES cholesterol from the tissues to the liver?
HDL
What is a skin lesion that contains CHOLESTEROL DEPOSITS called?
XANTHOMAS (GENETIC DISORDER)
What is an optimal LDL, HDL, total cholesterol?
<200, <100 and >60
What are the three types of athersclerotic lesions?
FATTY STREAKS, PLAGUE, COMPLICATED LESIONS
How can I modify hypertension and diabetes and reduce the risk of ATHERSCLEROSIS?
LIFESTYLE CHANGES, COMPLIANCE with MEDICATIONS
What is a macrophage laden with lipids called?
FOAM CELL
ARTERIAL DISEASE-EXTREMITIES

_____ _____ disease-atherosclerotic blockages?

-Large arteries, not heart, brain, aortic arch.

______ _______ (Buerger disease)

-non-sclerotic inflammation and thrombosis
-small and medium sized arteries and veins in foot and lower leg?

_______ _______ intense vasospasm?

-arteries and arterioles in fingers and occassionally toes?
PERIPHERAL ARTERY DISEASE

THROMBOANGIITIS OBLITERANS

RAYNAUD PHENOMENON
_____ _____ DISEASE?

-PATHO- ATHERSCLEROSIS, or inflammatory process.

-RISKS- men 60-70's, smoking, diabetes.

-GRADUAL onset

-CLINICAL MANIFESTATIONS: claudication, thinning of skin, decrease in size of leg muscles, numbness, leg color-dependent Rubor, blanches with elevation, ulceration, gangrene.

-DIAGNOSIS- physical exam, ankle to arm ration (<0.9 occlusion), ultrasound, MRI, arteriograms.

-TREATMENT- walking to point of claudification, reduce risks, avoid injury, meds, surgery
PERIPHERAL ARTERY DISEASE
_______ ______ (BUERGER DISEASE)?

-Non-sclerotic, inflammation/thrombosis of small and medium sized arteries and veins usually in feet, lower legs

-CAUSE- UNKNOWN

-RISKS- <35 years, heavy smokers

-CLINICAL MANIFESTATIONS: pain, intermittent claudification, increased sensitivity to cold, decreased pulses, thin shiny skin, with impaired hair/nail growth, tissue ulceration-gangrene

-DIAGNOSIS- Ankle/arm ratio, ultrasound, MRI, CT, arteriography

-TREATMENT- stop smoking, meds, surgery
THROMBOANGIITIS OBLITERANS
______ ______ RED, WHITE, BLUE DISEASE?

-Vasospasm- arteries, arterioles, usually occurs in hands/fingers

-CAUSE- UNKNOWN

-RISK FACTORS- young women, cold exposure, strong emotions

-CLINICAL MANIFESTATIONS- pallor(white)-cyanosis(blue),-hypermedia(red)-normal, color, cold, numbness, parenthesis(tingling)

-DIAGNOSIS- cold water immersion of hands, Doppler studies

-TREATMENT- eliminate cause, meds, surgery
RAYNAUD PHENOMENON
_______ localized area of vessel dilation caused by weakness in arterial wall?

TYPES:

-BERRY- occurs in the BRAIN (CIRCLE of WILLIS)

-FUSIFORM-

-DISSECTING- life threatening, tear in the lining of the Tunica Intima

-CLINICAL MANIFESTATIONS- depends on location, size

-DIAGNOSIS- MRI, CT, ULTRASOUND

-TREATMENT- surgical, reduce risk
ANEURYSMS
A client complains of pain in the calf when walking. The nurse understands this to be a symptom of what disorder? What causes the symptom?
CLAUDIFICATION

PERIPHERAL ARTERY DISEASE, BERGER'S DISEASE-STOP SMOKING
What arterial disorder primarily manifests in the HANDS and FINGERS?
RAYNAUD'S
What advice to reduce the risk of Raynaud's phenomenon would you provide to a client?
Buerger's?
AVOID COLD EXPOSURE

STOP SMOKING
Where do BERRY ANEURISMS commonly occur?
BRAIN
What are the clinical manifestations of a descending aortic dissecting aneurysm?
SEVERE BACK PAIN
______ pressure- ventricular contraction?
SYSTOLIC PRESSURE
_______ pressure- ventricular relaxation?
DIASTOLIC PRESSURE
______ ______ pressure- tissue perfusion pressure > greater than 70?
MEAN ARTERIAL PRESSURE
______ pressure - Systolic - Diastolic?
PULSE
_____ _____ - HR X STROKE VOLUME?
...
____ _____ PRESSURE- DIASTOLIC + (PULSE PRESSURE/3)?
MEAN ARTERIAL PRESSURE
______ PRESSURE - CO X TOTAL PERIPHERAL RESISTANCE?
BLOOD
MECHANISMS for ____ REGULATION?

-CARDIOVASCULAR CENTER-MEDULLA, PONS

-BARORECEPTOR and CHEMORECEPTOR REFLEXES

-CARDIAC OUTPUT

-PERIPHERAL VASCULAR RESISTANCE-LEFT SIDE-
AFTERLOAD

-NATRIURETIC PEPTIDES

-RENIN-ANGIOTENSINOGEN-ALDOSTERONE SYSTEM
B/P BLOOD PRESSURE
________ ______ substances released from increased stretch of the vessels?
NATRIURETIC PEPTIDES
_____ ____ ____ causes vasoconstriction, increased heart rate?
SYMPATHETIC NERVOUS SYSTEM
______ ____ ____ slows the heart rate?
PARASYMPATHETIC NERVOUS SYSTEM
_____ _____ CLASSIFICATIONS?

-Primary/Essential Hypertension-NO CAUSE can be identified (90-95%).

_____Risk factors-family history, race, age, metabolic syndrome

-Secondary hypertension-an elevation in blood pressure due to another disease (5-10%).

_____Causes-renal disease, disorders of adrenal hormones, pheochromocytoma

-Hypertensive crisis-systolic>180 or diastolic > 120 mm HG

-Orthostatic hypotension-abnormal drop in B/P when moving from a seated or supine position?
BLOOD PRESSURE
______/_____ _____ NO CAUSE can be identified (90-95%).
Primary/Essential Hypertension
_____ _____- an elevation in blood pressure due to another disease (5-10%).
Secondary hypertension
________ tumor of the adrenal gland?
pheochromocytoma
______ ______ systolic>180 or diastolic > 120 mm HG

Becomes an emergency in organ damage.
Hypertensive crisis
_____ ______ abnormal drop in B/P when moving from a seated or supine position?
Orthostatic hypotension
If I move too quickly from a reclining to standing position, what does my BARORECEPTOR REFLEX do?
Helps maintain blood pressure when going from a sitting to standing position.
If NATRIURETIC PEPTIDE is released, what will happen to my blood pressure?
GOES DOWN
What two actions occur in response to the release of ANGIOTENSIN II?
INCREASES IN VOLUME and PRESSURE
If CARDIAC OUTPUT INCREASES what will happen to blood pressure?
GOES UP
What happens to BLOOD PRESSURE in response to massive vasodilation?
Causes HYPOTENSION
_____ LESS THAN <120 and LESS THAN <80?
NORMAL BLOOD PRESSURE
_____ 120-139 OR 80-89?
PREHYPERTENSIVE
_____ ____ 140-159 OR 90-99?
STAGE I
____ _____ >160 OR >100
STAGE II
_____ _____ ______?

-HEART-HYPERTROPHY, MI (MYOCARDIAL INFARCTION) HEART FAILURE

-BRAIN-STROKE, TIA (TRANSIENT ISCHEMIC ATTACK)

-CHRONIC KIDNEY DISEASE

-PERIPHERAL VASCULAR DISEASE

-RETINOPATHY
TARGET ORGAN DAMAGE
_______ TREATEMENT?

-GOAL
--B/P<140/90
--DIABETICS, KIDNEY DISEASE < 130/80

-LIFESTYLE MODIFICATIONS
---WEIGHT
---SODIUM
---DASH DIET-LOW SODIUM
---ETOH
---EXCERCISE
---SMOKING CESSATION
---MAINTAIN Ca and K INTAKE

-MEDICATIONS

Dietary approaches to stop Hypertension-MEDITTERANEAN DIET.
HYPERTENSION
A patient complains of dizziness and lightheadedness upon getting up in the morning? What problem does the nurse expect?
ORTHOSTATIC HYPOTENSION
Give three examples of target organ damage that
can occur in association with uncontrolled hypertension?
HYPERTROPHY, STOKE, RETINOPATHY-BLINDNESS
A client presents to the Emergency Room with a B/P of 210/120 and complaints of a headache. What problem is represented?
HYPERTENSIVE CRISIS-SYMPTOMS OF IN ORGAN DAMAGE
A client has had repeated B/P ranging from 140-159/90-99. What is the B/P classification?
STAGE I HYPERTENSION
What is the treatment for hypertension?
Lifestyle modifications and medications
VENOUS DISORDERS

____ ____ dilated, tortuous VEINS of the lower extremities?
VARICOSE VEINS
____ ____ _____ VENOUS hypertension?
CHRONIC VENOUS INSUFFICIENCY
_____ _____ presence of a THROMBUS in a vein and the accompanying inflammatory response?
VENOUS THROMBOSIS
_____ ______?

-Primary - originates in SUPERFICIAL VEINS
-Secondary- impaired flow in deep veins

--RISK FACTORS: GENDER, AGE, OBESITY, PROLONGED STANDING, INCREASED INTRA-ABDOMINAL PRESSURE.

--CLINICAL MANIFESTATIONS: ACHING, EDEMA, PHYSICAL LOOK

--DIAGNOSIS: PHYSICAL EXAM, DOPPLER STUDIES, ANGIOGRAPHIC VENOUS STUDIES

--TREATMENT: IMPROVE FLOW, PREVENT INJURY
-----COMPRESSIONS/SUPPORT STOCKINGS
-----SCLEROTHERAPY
-----SURGICAL TREATMENT-DEEP VEIN
VARICOSE VEINS
SIGNS OF ______ ______ ______?

-EDEMA-INCREASED HYDROSTATIC PRESSURE IN THE VEINS

-VARICOSE VEINS

-SKIN CHANGES & DISCOLORATION

-SKIN ULCERATION

REFLUX OUTFLOW OF IMPAIRED MUSCLE PUMPS
CHRONIC VENOUS INSUFFICIENCY
_____ ____ ____ disorders originates in SUPERFICIAL VEINS?
Primary Varicose Veins Disorders
____ ____ ____ disorders impaired flow in deep VEINS?
Secondary Varicose Veins Disorders
SCLEROTHERAPY- ______ VEIN?
SUPERFICIAL
SURGICAL TREATMENT- _____ VEIN?
DEEP
_____ ______?

-VIRCHOW'S TRIAD- RISKS-CAUSES INCREASE RISK OF A VENOUS CLOT
---VENOUS STASIS-PULLING OF BLOOD TO CLOT
---INCREASED BLOOD COAGULABILITY
---VASCULAR WALL INJURY

-CLINICAL MANIFESTATIONS:
PAIN, SWELLING, DEEP MUSCLE TENDERNESS, SOME are ASYMPTOMATIC

-DIAGNOSIS: ULTRASOUND, VENOGRAPHY, LABS-D-DIMER

-TREATMENT:
---PREVENTION
---THROMBOLYTICS, ANTICOAGULATION
---BEDREST-GRADUAL AMBULATION (AVOID STANDING, SITTING) with support stocking.

-COMPLICATIONS: PULMONARY EMBOLISM
VENOUS THROMBOSIS
What are the three elements of VIRCHOW'S TRIAD and give one example of each?
VENOUS STASIS-IMMOBILITY, BED REST, VENOUS OBSTRUCTION

INCREASED BLOOD COAGULABILITY-ORAL CONTRACEPTIVES, STRESS, TRAUMA, PREGNANCY

VASCULAR WALL INJURY-SURGERY, HIP FRACTURES, INDWELLING VENOUS CATHETER
Why are nurses at risk for the development of varicose veins?
PROLONG STANDING
What is the pathophysiologic basis for the brown, discoloration of skin that is seen in VENOUS INSUFFICIENCY?
HEMOCIDERIN-BREAKDOWN OF RED BLOOD CELLS
Why do VENOUS STASIS ULCERS develop?
Decrease diffusion of gases across the edema prevents healing from happening.
What complication is a client with a DEEP VEIN THROMBOSIS at RISK for?
PULMONARY EMBOLISM
______ ______ DISEASE?

-Disease of heart as a result of impaired coronary blood flow

-Two main coronary arteries branch off the aortic root
_____ Left-Left anterior descending-circumflex

_____ Right-Posterior descending

-Most common cause of CAD is atherosclerosis
CORONARY ARTERY DISEASE
Most common cause of CAD is ________?
Atherosclerosis
CAD-________?

-SYMPTOM-of coronary artery disease

-PAIN

-TYPES-

___CHRONIC STABLE/EXERTIONAL

___VARIANT (PRINZMETALS, VASOSPASTIC)

___UNSTABLE ANGINA
ANGINA
CAD_______?

-Sudden onset of pain or pressure in chest

-Not all patients with coronary artery disease will have angina

-LOCATION: SUBSTERNAL AREA, may RADIATE to BACK, LEFT SHOULDER, JAW, ARMS.

-CHRONIC STABLE ANGINA- Relieved with rest, or NITROGLYCERIN
ANGINA
______ ______ _____ Relieved with rest, or NITROGLYCERIN?
CHRONIC STABLE ANGINA
CAD- ______ _____?

-PAIN-
___Occurs at rest or with minimal exertion

___Lasts more than 20 minutes if untreated

___Severe-described as frank pain and of new onset

___More severe, prolonged, than previously
experienced
UNSTABLE ANGINA
DIAGNOSIS/TREATMENT- _______?

-HISTORY/PHYSICAL-risk actors, pain

-LAB STUDIES- LIPID PANEL

-DIAGNOSTICS TESTS-EKG, ECHO, EXERCISE STRESS TESTING, CT, MRI, CARDIAC CATH

-TREATMENT-REDUCE SYMPTOMS

-----PHARMACOLOGIC - MEDS
-----CORONARY INTERVENTIONS-PCI, percutaneous coronary intervention (PCI), CABG Coronary artery bypass grafting (CABG
-----NON-PHARMACOLOGIC-REDUCE RISK FACTORS
CAD (CORONARY HEART DISEASE)
____ _____ _____?

-TYPES OF LESIONS-

-----Fixed, stable plague
-----UNSTABLE PLAGUE

-COMPLICATIONS-

-----ANGINA
-----THROMBUS FORMATION
-----MYOCARDIAL INFARCTION
CORONARY ARTERY DISEASE
_____ ____ _____?

-SPECTRUM-UNSTABLE ANGINA to ACUTE MI

-To determine if an MI has occurred, what is happening to the myocardium is observed through

---EKG changes

---SERUM BIOMARKERS
-----TROPONIN I (TnI)
-----TROPONIN T (TnT)
-----CREATININE KINASE (CK-MB)
-----MYOGLOBIN
ACUTE CORONARY SYNDROME
_____ _____?

-UNSTABLE ANGINA-

-----ANGINA, causes ischemia but no elevation in serum markers

-NON-ST ELEVATION MI

-----Unstable angina where ischemia is severe and causes myocardial damage
-----Serum markers are detected
-----Partial thickness damage occurs

-ST elevation MI

-----Necrosis of the myocardial tissue
-----Area of infarction determined by affected coronary artery
-----Full thickness damage occurs
MYOCARDIAL INFARCTION
_____ _____ RELATED TO VESSEL OCCLUDED?
MI (MYOCARDIAL INFARCTION)
PATHOPHYSIOLOGY of _____ _____?

-Lack of blood flow to myocardium
-Aerobic to anaerobic metabolism - inadequate energy produced to sustain function
-Loss of contractile function
-Cell damage within 40 minutes
-Necrosis - 20-40 minutes of severe ischemia
-Three zones of tissue damage
-----Necrotic Zone
-----Surrounding zone of injured/hypoxic cells-some recovery
-----Ischemic - Salvageable cells
-Inflammation, phagocytosis of necrosis, formation of granulation tissue
-Replacement of necrotic cells with collagen, scar tissue (decreased function)
MYOCARDIAL INFARCTION
CLINICAL MANIFESTATIONS OF _____ ____ ____?

-Chest pain - angina
-----Severe, crushing, constrictive

-Sympathetic nervous system response
-----GI distress, nausea, vomiting
-----Tachycardia, Vasoconstriction
-----Anxiety, restlessness, impending doom

-Hypotension and shock
ACUTE MYOCARDIAL INFARCTION
EKG Changes - _____?

-EKG changes

-----ST SEGMENT ELEVATION
-----T WAVE INVERSION
-----ABNORMAL Q WAVE
STEMI
_____ ______?

-SERUM BIOMARKERS
---Troponin assays (Troponin I (Tnl), Troponin T (TnT)
-----Present in cardiac muscle
-----Increase within 3 hours after onset and remain elevated 7-10 days

-CREATININE KINASE (CK-MB)z
---Found in all muscle cells
---MB isoenzyme specific to myocardial tissue
---Increase within 4-8 hours after onset peaks at 24 hours and remains elevated for 2-3 days

-Myoglobin
---Not specific to cardiac injury
---Carries oxygen to myocardial, skeletal muscle
---Increased within 1 hour after cell death, peaks in 4-8 hours
SERUM BIOMARKERS
TREATMENT - _______ ______?

---THROMBOLYTICS
-----LYSE THROMBUS

---Percutaneous coronary intervention (PCI) with stent placement
-----Unstable angina/Non-STEMI

-Coronary artery bypass graft (CABG)
-----Surgical revascularization
REPERFUSION THERAPY
COMPLICATIONS ______ ______?

-----Sudden cardiac death
-----Cardiogenic shock
-----Heart Failure
-----Arrhythmias
-----Ventricular, valve, interventricular septal rupture (greatest risk- 3-7days post injury)
-----Pericarditis
-----Aneurysms
_____Stoke
MYOCARDIAL INFARCTION
What are to modifiable and two non-modifiable risk factors associated with coronary artery disease?
DIET, EXERCISE

GENETICS, GENDER
What question would you ask a client to assess for angina?
Are you having pain?
Which type of angina is caused by vasospasm?
VARIANT
What would you advise a client who experiences angina while walking to do?
STOP, SIT DOWN and REST
What EKG change is associated with acute myocardial ischemia?
ST SEGMENT ELEVATION
An elevation in what lab value would be most indicative of an MI?
TRIPONIN
_____ _____ ______?

PATHO: Infection of the inner surface of the heart and valves

BACTERIAL INVASION: Valvular vegetation - emboli - bacteremia - destruction of cardiac tissue - dysfunction of valves

RISKS: Dental/Surgical procedure (Portal of Entry), IV drug use, diabetes, neutropenia, damaged endocardial surface (valvular disease).

Common infecting organisms-staphylococcal, streptococci, enterococci

COMMON SITE - AORTIC, MITRAL VALVES

CLINICAL MANIFESTATIONS: FEVER, HEART MURMUR, PETECHIAL HEMORRHAGES in SKIN, NAILBEDS, MUCOUS MEMBRANES, COUGH ARTHRALGIA/ARTHRITIS (EMBOLI)

DIAGNOSIS: BLOOD CULTURE, ECHOCARDIOGRAM

TREATMENT: ANTIBIOTICS, may require VALVE REPLACEMENT, PROPHYLAXIS for PREDISPOSING CONGENTIAL VALVE DISORDERS
ACUTE INFECTIVE ENDOCARDITIS
_____ _____ - _____, _______?

-Heart valves promote unidirectional flow of blood through the heart

-Causes of disorders: Congenital, Trauma, Ischemia, Infection, Inflammation

-Most Common: MITRAL, AORTIC

-STENOSIS - Narrowing of orifice, failure of leaflets to open normally-turbulence-decreased blood flow-impaired emptying, increased work demands on heart

-REGURGITANT VALVE- does not close-properly-blood flow continues despite valve closure or backward flow
VALVULAR DISEASE - STENOSIS, REGURGITATION
_______ _______?

-HEART MURMUR

-----STENOSIS- Hear murmur when blood shoots through the narrow opening when valve opens

-----REGURGITATION-When blood leaks back through a valve that should be closed

-Mitral regurgitation, stenosis, aortic regurgitation
---PULMONARY SYMPTOMS

-AORTIC STENOSIS - angina, syncope and heart failure

-
VALVULAR DISEASE
What two tests are used to diagnose infective endocarditis?
CULTURE and ECHO
Abnormal turbulent blood flow through a diseased valve produces what clinical manifestation?
MURMURS
What happens to blood flow in diastole in mitral valve stenosis?
Less flow, less filling of the left ventricle
What happens to the left ventricle in aortic valve stenosis?
HYPERTROPHY
Does mitral valve regurgitation result in a decreased stroke volume?
Yes, stroke volume - the amount of blood ejected from the ventricle with each beat.
What valvular problem does the nurse anticipate if the chordae tendinae rupture as a complication of MI?
Mitral Valve Regurgitation
________?

-Inflammation of the PERICARDIUM

-Causes: Infectious non-infectious process

-PATHO: Vasodilation, increased capillary permeability, WBC's, exudate in pericardial space

-CLINICAL MANIFESTATIONS: CHEST PAIN, - PLEURITIC/POSITIONAL FEVER, PERICARDIAL FRICTION RUB, EKG CHANGES

-DIAGNOSIS: EKG, ECHO, CXR, LABS

-TREATMENT: BASED ON CAUSE

-COMPLICATIONS - Pericardial effusion tamponade, adhesions/scar tissue
PERICARDITIS
______ _____?

-PERICARDIAL TAMPONADE - life threatening compression of the heart due to blood/fluid in pericardial space

-CLINICAL MANIFESTATIONS: JUGULAR VEIN DISTENSION, NARROWING of PULSE PRESSURE, MUFFLED HEART SOUNDS, TACHYCARDIA, PULSUS PARADOXUS (FALL IN B/P with INSPIRATION)

TREATMENT- PERICARDIOCENTESIS
CARDIAC TAMPONADE
______ ______ life threatening compression of the heart due to blood/fluid in pericardial space
PERICARDIAL TAMPONADE
________?

-Disorders of heart muscle

-Primary and Secondary causes

-Types-

-----HYPERTROPHIC
-----ARRHYTHMOGENIC
-----RIGHT VENTRICULAR DYSPLASIA
-----DILATED
-----RESTRICTIVE
-----PERIPARTUM
CARDIOMYOPATHY
_____ _______?

-PATHO: Left ventricular hypertrophy, disproportionate thickening of the ventricular septum-abnormal filing, cardiac arrhymias, outflow obstruction (left ventricle-in 25%)

-GENETIC DISORDER: Autosomal dominant, genetic mutation

-CLINICAL MANIFESTATIONS: DYSPNEA, CHEST PAIN, SYNCOPE (POST-EXERTION), ATRIAL FIBRILLATION, VENTRICULAR ARRHYTMIAS (POST-EXERTIONAL)

-DIAGNOSIS: ECHOCARDIOGRAM, EKG, CONTINUOUS AMBULATORY MONITORING (HOLTER MONITOR), MRI, GENETIC TESTING, PHYSICAL EXAM MAY BE NORMAL

-TREATMENT: MEDICAL MANAGEMENT, MEDICATIONS, PACEMAKERS, AICD; SURGICAL - MYECTOMY/ABLATION of SEPTUM
HYPERTROPHIC CARDIOMYOPATHY
_______ Global standards for myocardium injury?
TROPONINS
_______ NOT REVERSIBLE?
NECROSIS
_____ _____ NEVER TO BE RETURNED?
NECROTIC ZONE
______ ______ CANNOT BE REPLACE, IT IS REPLACED BY SCAR TISSUE?
MYOCARDIAL CELLS
___ ______ _____ IN THE PRESENCE OF ACUTE INJURY?
ST SEGMENT ELEVATES
___ _____ _____ AS A RESULT OF INJURY TO MYOCARDIAL CELLS?
ST ELEVATION MI
_______ - PROMINENT T WAVE?
NECROSIS
______ ______ the difference between the end-diastolic and end-systolic volumes (approximately 70 mL) is called?
STOKE VOLUME
_________ the ability of a cell to depolarize itself, reach threshold potential, and produce a propagated action potential; cells with this capability are called automatic cells?
AUTOMATICITY
________ _______ ________ a resistance to the flow of blood determined by the tone of the vascular musculature and the diameter of the blood vessels. It is responsible for blood pressure when coupled with stroke volume?
Peripheral Vascular Resistance
________ the obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue?
INFARCTION
______ A type of chest pain caused by reduced blood flow to the heart?
ANGINA
________inotropic agents weaken the force of muscular contractions? Positively inotropic agents increase the strength of muscular contraction?
Negative
________ inotropic agents increase the strength of muscular contraction?
Positive
______ ________is the difference between the systolic and diastolic pressure readings?

It is measured in millimeters of mercury (mmHg). It represents the force that the heart generates each time it contracts. If resting blood pressure is (systolic-diastolic) 120-80 millimeters of mercury (mmHg), pulse pressure is 40.
PULSE PRESSURE
_________ is the increase in the volume of an organ or tissue due to the enlargement of its component cells?
HYPERTROPHY
In vascular diseases, _________ _________is a systemic pathological state of the endothelium (the inner lining of blood vessels) and can be broadly defined as an imbalance between vasodilating and vasoconstricting substances produced by (or acting on) the endothelium?
ENDOTHELIUM DYSFUNCTION
__________a receptor sensitive to changes in pressure?
BARORECEPTOR
______ _______A small aneurysm that looks like a berry and classically occurs at the point at which a cerebral artery departs from the circular artery (the circle of Willis) at the base of the brain. Berry aneurysms frequently rupture and bleed?
BERRY ANUERYSM
______ _______ An irregular shaped widening of a cerebral vessel that does not have a discrete neck or pouch of the side of a vessel. Fusiform aneurysms may rupture, press on brain stuctures, or cause strokes?
FUSIFORM ANEURYSM
_____ ______ An aneurysm in which the wall of an artery rips (dissects) longitudinally. This occurs because bleeding into the weakened wall splits the wall. Dissecting aneurysms tend to affect the thoracic aorta. They are a particular danger in Marfan syndrome?
DISSECTING ANEURYSM
_____ ______ appear as thin yellow lines running along the major arteries, such as the aorta.
FATTY STREAKS
The _____ _____ is the basic lesion of clinical atherosclerosis.
FIBROUS PAQUE
_____ ______ develop when the fibrous plaque breaks open, producing hemorrhage, ulceration, and scar tissue deposits?
COMPLICATED LESIONS
The resistance to left ventricular ejection and myocardial contractility all affect stroke volume?

THE RESISTANCE TO EJECTION OF BLOOD FROM THE VENTRICLES

THE PRESSURE OR TENSION WORK OF THE HEART
AFTERLOAD
The amount of blood in the left ventricle at the end of diastole is ______?

OR VENTRICULAR FILLING
PRELOAD
END-DIASTOLIC PRESSURE _______?

VOLUME WORK OF THE HEART
PRELOAD
_____ the ability of the cardiac tissue to respond to action potentials?
conductivity
________ electrical activation of a cardiac cell?
DEPOLARIZATION
______ deactivation of cardiac cell with reestablishment of the resting membrane potential?
REPOLARIZATION
____-____ ____: the greater the stretch of cardiac muscle fibers, the greater the force of contraction?
FRANK=STARLING LAW
____ ____ OUTERMOST, made up of collagen and provides a protective covering for blood vessel?
TUNICA EXTERNA
____ ____ Made up of SMOOTH MUSCLEs, promotes the ability for blood vessel to expand and contract; vasodilate and vasoconstrictor in relation to blood flow
TUNICA MEDIA
___ ____ INNER MOST, ENDOTHELIAL CELLS line inner layer of tunica intima, play an important role in the validity of the blood vessel themselves and damage to this layer is what lays the ground work for the problems we have in a vascular perspective?

EX: CORONARY ARTERY & PERIPHERAL ARTERY DISEASE
TUNICA INTIMA
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