Chapter 33: Alterations Of CV Function Flashcards
Prevalence of CV dz
Leading cause of death in the United States and the world
Total percent of deaths from cardiovascular diseases in the United States: 24.6%
Develop from lifestyle choices: sedentary, smoking, diet
Mechanisms of CV dz
Genetic, neurohumoral, and inflammatory mechanisms:
Underlying tissue and cellular processes ->
Endothelial injury
Remodeling
Stunning -> plaque forms and cannot perfuse
Reperfusion injury
Inflammation
Varicose veins
Vein in which blood has pooled
Usually in the saphenous vein
Distended, tortuous, and palpable veins
Causes of VV
Trauma or gradual venous distention, rendering valves incompetent
Think pressure and weight
RF of VV
genetic predisposition, pregnancy, obesity, prolonged sitting or standing,
Manifestations of VV
Irregular, purplish, bulging veins
Pedal edema
Fatigue
Aching in the legs
Shiny, pigmented, hairless skin on the legs and feet
Skin ulcer formation
Dx of VV
physical examination, Doppler ultrasound, and venogram
tx of VV
rest with affected leg elevated, compression stockings, avoid prolong standing or sitting, exercise, sclerotherapy, and surgical removal
Chronic venous insufficiency
Inadequate venous return over a long period as a result of varicose veins and valvular incompetency
Manifestations of CVI
Lower-Leg swelling, skin color and texture changes -> yellow slough or ruddy skin, venous ulcers (ankles) with irregular borders, dull, achy pain, pulse present, drainage
Deep vein thrombosis
Thrombosis: Clot
Detached thrombus: Thromboembolus; can lead to pulmonary emboli
Clot in a large vein
Obstruction of venous flow leading to increased venous pressure
Virchow triad: DVT
Venous stasis:
Immobile -> sx, long airplane ride, VV, obesity
Venous endothelial damage:
Sx, trauma, VP, atherosclerosis
Hypercoagulable states:
Genetic, malignancy, oral contraception, smoking
Common places of DVT
Typically see in legs, pelvis is hospitalized pt, arms in sedentary person
Prevention of DVT
Mobilization soon after surgery, illness, bed rest, injury
Prophylactic low–molecular-weight heparin, antithrombin agents, warfarin, or pneumatic devices
Inferior vena cava filter -> screen placed in IVC to catch clots
Dx of DVT
D-dimer: test that looks at fibrin degradation products (FDPS) in the blood –increased = blood clot formation
US
Tx of DVT
Low–molecular-weight heparin, unfractionated intravenous heparin, antithrombin agents, or adjusted-dose subcutaneous heparin
Thrombolytic therapy: TPA
Aspirin: Antiplatelet
HTN
Prolonged elevation in blood pressure
Excessive cardiac workload due to increased afterload and vasoconstriction
RF for HTN
advancing age, ethnicity (AA and Hispanic), family history, being overweight or obese, physical inactive, tobacco use, high-sodium diet, excessive alcohol intake, stress, and other chronic conditions
Primary HTN
Most common form
Develops gradually over time
Causes of primary HTN
Essential or idiopathic
Secondary HTN
Tends to be more sudden and severe
Occurs secondary to another cause
Causes of secondary HTN
Causes: renal disease, adrenal gland tumors, certain congenital heart defects, certain medications, and illegal drugs, pregnancy dt estrogen
Malignant HTN
Intensified form
Does not respond well to treatment
Manifestations of HTN
“Silent killer”
Include: fatigue, headache, malaise, and dizziness
Most common cause of stroke
HTN
Complications of HTN
atherosclerosis, aneurysms, MI, heart failure, stroke, hypertensive crisis, renal damage, vision loss, metabolic syndrome, memory problems
HTN encephalopathy: confusion, HA, sz
HTN retinopathy
HTN cardiomyopathy: HF
HTN nephropathy: chronic RF
HTN crisis
180/120. Typically bc patient is not treating their BP
Dx of HTN
history, physical examination, multiple blood pressure readings at varying times of the day,
Tx of HTN
Early detection and management is essential to prevent complications
Pharmacologic treatments
Restrict diet to 2g/1 teaspoon NA, Dash diet, stop smoking, exercise
DASH diet
6-8 servings of grains per day
6 or less servings of lean protein per day
4-5 servings of fresh fruits and veg per day
4-5 servings of legumes or nuts/seeds per day
Limited fats and sweets
2-3 servings of low-fat dairy per day
Orthostatic (postural) hypotension
Decrease in the systolic and diastolic blood pressures on standing by SBP 20 mm Hg or more and by DBP 10 mm Hg or more, respectively
Lack of normal blood pressure compensation in response to gravitational changes on the circulation, leading to pooling and vasodilation
Acute vs. chronic
Acute orthostatic hypotension
Caused by certain antiHTN medications.
Manifestations of ortho hypotension
Fainting upon standing
Typically occurs in an older person with lack of vaso motor tone. When they stand up, all the blood goes tot heir feet instead of vasoconstriction and keeping blood up in core.
Tx of ortho hypotension
Liberalize salt intake, raise the head of the bed, wear thigh-high stockings, expand volume with mineralocorticoids (aldosterone), and administer vasoconstrictors (shunt blood to core and head)
Aneurysms
Weaken of an artery
Can occur in an artery: Common in the abdominal aorta (most common), thoracic aorta, and the cerebral (second most common), femoral, and popliteal arteries
Can rupture – exsanguination
True and false aneurysms
RF for aneurysms
congenital defect, atherosclerosis, hypertension, dyslipidemia, diabetes mellitus, tobacco, advanced age, trauma, and infection
3 types of true aneurysms
affect all three vessel layers
Saccular aneurysm – bulge on the side
Cerebral
Fusiform aneurysm – occurs the entire circumference
Aortic
Dissecting aneurysms - occurs in the inner layers
Inner layer breaks open an bleeding starts in the layers
Fast leak -> emergency sx
Slow leak -> manage with BP medications
False aneurysm
does not affect all three layers of the vessel
3 things to think for aneurysm
- Where is it located
- True or false
- Shape
Manifestations of aneurysm
Aortic aneurysm asymptomatic until it ruptures -> pulsating mass, tearing pain
thoracic aorta -> resp difficulty.
Neuro decline common in brain aneurysm -> sz, sudden headache, loss of consciousness.
An extremity could be impaired.
Rupture -> shock -> sx
Dx of aneurysm
physical examination, X-ray, echocardiogram, CT, MRI, and arteriography
Tx of aneurysm
eliminating or managing cause and surgery
Thrombus
Stationary blood clot.
Activation of the coagulation cascade.
Causes of thrombus
roughening of the tunica intima by atherosclerosis
Emboli
Emboli – traveling body
May be a thrombus, air, fat, tissue, bacteria, amniotic fluid, tumor cells, and foreign substances
Can become lodged in places like the lungs, brain, and heart
Peripheral vascular dz
Narrowing of the peripheral vessels
Decreased blood supply to extremities
Causes of PVD
atherosclerosis, thrombus, inflammation, and vasospasms
Raynauds dz
Vasospasms of arteries, usually in the hands, because of sympathetic stimulation
Associated with autoimmune dz
Thomromboangitis obliterans - Bergers disease
An inflammatory condition of the arteries
Rare but BV inflamed and they swell and when they swell they’re blocked with clots -> necrosis, could gangrene
Common cause of BD
Smoking
Manifestations of PVD
pain, intermittent claudication, numbness, burning, non-healing wounds, skin color changes, hair loss, and impotency, black Eschar, round smooth sores on toes and feet, NO drainage or edema, cool to touch
“The pain gets better if I dangle my foot of the bed -elevating my feet makes the pin worse”
Intermittent Claudication: first s/sx, c/o pain and heaviness in legs, induced by exercise and relieved by rest.
Shiny, hairless skin
No pulse
Dx of PVD
US or arteriography would be the most definitive: dye into artery and see how patent.
tx of PVD
reducing contributing factors, angioplasty, bypass procedures, laser procedures, atherectomy, antiplatelet agents (clopidogrel), anticoagulants, thrombolytic, and lipid-lowering agents
Stop smoking!!!
Exercise -> walk 1 hr/day to stimulate collateral circ around those vessels. Can rest with pain, but restart
Weight reduction
Control DM and hyperlipidemia
If nothing else works -> amputation
Dyslipidemia
High levels of lipids in the blood
Increases risk for many chronic diseases
Lipids come from dietary sources and liver production
Dietary sources
Cholesterol – animal products
Triglycerides – saturated fats
Very common
Types of cholesterol
Classified based on density, which is based on the amount of triglycerides (low density) and protein (high density)
Very-low density lipoproteins
Low density lipoproteins AKA “bad” cholesterol -> lead to deposition of plaque in BV
High density lipoproteins – AKA “good” cholesterol
HDL grab LDL and take them to liver to eliminate them
Manifestations of hyperlipidemia
asymptomatic until it develops into other diseases
Dx of hyperlipidemia
cholesterol screening and lipid panels
Tx of hyperlipidemia
dietary changes, weight reduction, routine exercise, tobacco cessation, lipid-lowering agents, and complication management
Atherosclerosis
Chronic inflammatory disease characterized by thickening and hardening of the arterial wall
Inflammatory process is triggered by a vessel wall injury -> HTN, smoking, hyperlipidemia, hyperhomocysteinmia, Hemodynamic factors, toxins, viruses, immune rxn
Lesions develop on the vessel wall and calcify over time
Leads to vessel obstruction, platelet aggregation, and vasoconstriction
Leading case of heart dz, contributes to stoke
Occurs throughout body
Mechanism of atherosclerosis
LDL enters vessel -> oxidized to inflammatory lipids and then these lipids causes adhesions and then these cells turn into foam cells and they cause fatty streak and fibrous plaque, they oxidize and lesions form and blood clots form on it.
Complications of atherosclerosis
peripheral vascular disease, coronary artery disease, thrombi, hypertension, and stroke
Manifestations of atherosclerosis
asymptomatic until complications develop
Dx of atherosclerosis
identify contributing factors and complications
Tx of atherosclerosis
similar to dyslipidemia with the addition of angioplasty, bypass, laser procedures, and artherectomy
Coronary artery dz
Atherosclerotic changes of the coronary arteries
Impairs myocardial tissue perfusion
Angina – chest pain resulting from myocardium ischemia
Infarction – necrotic damage to the myocardium
Causes of CAD
atherosclerosis, vasospasms, thrombus, and cardiomyopathy
Complications of CAD
myocardial infarction, heart failure, dysrhythmias, and sudden death
Manifestations of CAD
angina, indigestion-like sensation, nausea, vomiting, clammy extremities, diaphoresis, and fatigue
Dx of CAD
H&P, identify contributing factors, exercise stress test, echocardiogram, and electrocardiogram
Tx of CAD
similar to those used to treat dyslipidemia and atherosclerosis with the addition of nitrates, vasodilators and anti-hypertensive’s, and oxygen
Angina
Intermittent chest pain resulting from myocardium ischemia
Stable – goes away with demand reduction
Goes away with nitro and rest
Unstable – increased intensity or frequency, does not go away with demand reduction, or occurs at rest
Medical emergency
Prizmentals Angina (variant angina)-occurs almost exclusively at rest
Caused by vasospasm with or without atherosclerosis
Coke, genetic
Infarction
permanent necrotic damage to the myocardium
MI
Death of the myocardium
Coronary artery blood flow is blocked due to atherosclerosis, thrombus, or vasospasms
Risk factors are the same as those for atherosclerosis
Manifestations of MI
Some are asymptomatic – “Silent” MI
Includes: angina, fatigue, nausea, vomiting, shortness of breath, diaphoresis, indigestion, elevation in cardiac markers, ekg changes
Infarcted myocardium is surrounded by a zone of hypoxic injury, which may progress to necrosis or return to normal; adjacent to this zone is a zone of reversible ischemia.
Sudden severe chest pain
ECG changes
Troponin I: Most specific
Elevates in 2 to 4 hours
Creatine phosphokinase–MB (CPK-MB), LDH
2 major types of MI
Subendocardial infarction (NSTEMI)
Transmural infarction (STEMI): Goes all the way through the myocardium
Coronary syndrome
Unstable Angina- Pre infarction. Can have ST changes on ekg, but cardiac enzymes are normal
Non- STEMI- Smaller infarctions are not associated with ST segment elevations
Suggest that additional myocardium is still at risk for recurrent ischemia and infarction
ST segment elevations (STEMI) on the ECG requires immediate intervention.
Individuals at highest risk for complications
EKG alterations for unstable angina and NSTEMI
St depression and t wave inversion
EKG changes for zones of MI
Zone of ischemia: st segment depression with or without t wave inversion as a result of altered repolarization
Zone of injury: myocardial injury cases ST segment elevation with out without loss of R wave
Zone of infarction: MI causes deep Q waves as result of absence of depolarization current from dead tissue and receding currents from opposite side of heart
Tx of MI
Hospitalization
Immediate administration of supplemental oxygen and aspirin -> anti plt an the chew it and within 10 min -> anti plt aggregation occurs.
Nitroglycerine -> vasodilation
Morphine -> pain
Beta Blockers > decrease HR and vasodilation
Anticoagulants -> warfarin or aixaban to prevent clotting
Bed rest
Thrombolytic candidate -> only STEMI
Percutaneous coronary intervention (PCI) -> NSTEMI and unstable angina
Surgery
Pericarditis
Inflammation of the pericardium
Fluid accumulates - pericardial effusion
Swollen tissue creates friction
Cause of pericarditis
Virus -most common
Open heart sx
Constrictive pericarditis
Loss of elasticity
Results from chronic inflammation
Cardiac tamponade
Cardiac compression from excessive fluid accumulation
Life-threatening
Manifestations of cardiac tamponade
Manifestations: falling arterial pressures fall, rising venous pressures, narrowing pulse pressure, and muffled heart sounds
decrease CO, low BP, increase preload
Complications of cardiac tamponade
heart failure, shock, and death
Manifestations of pericarditis
Pericardial friction rub (grating sound heard when breath is held)
Sharp, sudden, severe chest pain that increases with deep inspiration and decreases when sitting up and leaning forward
Dyspnea
Tachycardia
Edema
Flulike symptoms
Dx of Pericarditis
H&P, CBC, electrocardiogram, chest X-ray, echocardiogram
Tx of pericarditis
identify and resolve the underlying cause,
nonsteroidal anti-inflammatory drugs, analgesics,
bed rest,
oxygen therapy, pericardiocentesis
pericardiectomy
Infective endocarditis
Commonly caused by Streptococcus and Staphylococcus infections
Vegetation forms on internal structures and creates small thrombi
Micro emboli occur as they are dislodged, resulting in micro-hemorrhages
RF for IE
intravenous drug use, valvular disorders, prosthetic heart valves, rheumatic heart disease, congenital heart defects
IE manifestations
flulike symptoms, fever, embolization, heart murmur, petechiae, splinter hemorrhages, Janeway lesions, Osler’s nodes, Roth spot on retina
Dx of IE
H&P, blood cultures, CBC, urinalysis, erythrocyte sedimentation rate, electrocardiogram, and echocardiogram
Tx of IE
identification of causative agent, long-term AB, bed rest, antipyretics, surgical valve repair, and prosthetic valve replacement
Valvular dz
Disrupt blood flow through the heart
Stenosis
narrowing
Less blood can flow through the valve
Causes decreased cardiac output, increased cardiac workload, and hypertrophy
Regurgitation
insufficient closure
Blood flows in both directions through the valve
Causes decreased cardiac output, increased cardiac workload, hypertrophy, and dilation
Causes of valve dz
congenital defects, infective endocarditis, rheumatic fever, myocardial infarction, cardiomyopathy, and heart failure
Manifestations of valve dz
Vary depending on valve involved
Reflect alteration in blood flow through the heart
dx of valve dz
H&P, heart catheterization, chest X-rays, echocardiogram, electrocardiogram, and MRI
Tx of valve dz
diuretics, anti-dysrhythmics, anti-hypertensives, anticoagulants, oxygen therapy, low-sodium diet, surgical valve repair, and prosthetic valve replacement
Cardiomyopathy
Conditions that weaken and enlarge the myocardium
Classified into three groups—dilated, hypertrophic, and restrictive
Dilated cardiomyopathy
Dilated is most common. Heart muscle dilates. Most are idiopathic, ischemia, MI, CAD, alc, pregnancy, drug use
Hypertrophic cardiomyopathy
septum thicken. genetic -> autosomal dominant disorder. Usually goes into sudden cardiac death.
Restrictive cardiomyopathy
muscle can’t relax, diastole dysfunction. Amyloidosis -> buildup of protein or fat in heart, build up of iron in heart
S/sx of cardiomyopathy
S/sx of heart failure: fatigue, dspneic, activity intolerance.
Tx of cardiomyopathy
Heart transplant
Heart failure
1 case of hospital admissions in age 65 and older
Inadequate pumping
Leads to decreased cardiac output, increased preload, and increased afterload
Compensatory mechanisms activated
Activation of the sympathetic nervous system
Activation of the renin-angiotensin-aldosterone system
Ventricular hypertrophy
Types of HF: systolic dysfunction
Systolic dysfunction:
Pump problem
HFrEF: Heart failure with reduced ejection fraction -> Decreased contractility, enlarged ventricles, results from reduced contraction of the L ventricle such that not enough blood is pumped into circ
types of HF: dastolic dysfunction
Filling problems
HFpEF: heart failure with reserved EF, decreased filling, thicken vent mm, L vent becomes stiff and does not relax normally, as a result it cannot fill properly and pressure begins to increase in the L heart chambers and in the lungs
Left-sided HF
Cardiac output falls
Blood backs up to the pulmonary circulation
Causes f L HF
left ventricular infarction, hypertension, and aortic and mitral valve stenosis
Manifestations of L HF
pulmonary congestion, dyspnea, and activity intolerance, lung cracked, wheezing, displaced cardiac apex, L sided heart murmurs
Right-sided HF
Blood backs up to the systemic circulation
Causes of R HF
pulmonary disease, left-sided failure, and pulmonic and tricuspid valve stenosis
Manifestations for RHF
edema and weight gain, hepatomegaly, increase JVD, regurgitant murmur in tricuspid area
Mixed dysfunction HF
Both systolic and diastolic dysfunction
HF manifestations
Shared L and R sx: cool peripheries, cyanosis, orthopnea, delayed cap refill
May be acute or chronic
Manifestations:
Depend on type
Fluctuates in severity
Appear as compensatory mechanisms fail
Includes: indications of systemic and pulmonary fluid congestion
HF dx
H&P, chest X-ray, echocardiogram, electrocardiogram.
HF tx
Identify and manage underlying cause
Include: lifestyle modification, angiotensin-converting enzyme inhibitors, diuretics, anti hypertensives, biventricular pacemaker, and heart transplant
