Exam #2: Cardiac Flashcards
What are the 4 common cardiac diagnostic test, and what does each do?
- EKG/ ECG: Electrocardiogram: Conduct electrical activity of the heart
- Echocardiogram Ultrasound of the heart: Changes in heart structure of function, valve, congenital
- Stress Test: checking for exercise induced problems such as arrhythmias
- Cardiac Catheterization: Visualize the inside of the coronary arteries look for blocked arteries and clear them out to restore blood flow
What is hypertension and when does it occur, what effects it?
Blood pressure greater than 140/90
Increases with age
African ancestry
Genetic factors
Sodium intake
Excessive alcohol usage
Obesity
Smoking
Prolonged or recurrent stress
Fluid
More common in men
What are we seeing in teenagers right now?
Hypertension, Type 2 Diabetes, Bad Diet, Poor Lifestyle choices
Cardiomeagly
Enlarged heart because it. Is working harder
What are the three major categories of hypertension?
Primary or essential: idiopathic
Secondary: typically results from renal or endocrine disorders
Tertiary: Usually results in target organ damage by reducing blood flow to the tissues
Why do we care if one has hypertension?
Straining on the heart
Pathophysiology of Primary hypertension
Increase in anterior vasoconstriction- increase workload of the heart- vasoconstriction-decrease blood flow to kidneys
Over long period of time pressure damages to arterial walls- sclerosis (hardening) of walls which become subject to injury- decreases lumen size for blood flow
Blood supply to involved area is reduced - ischemia and necerosis of tissues with loss of function
Walls are smooth muscle
What does hypertension do the brain?
Cerebral aneurysm hemorrhagic CVA Stoke
What does hypertension do the eyes?
Retinopathy, arteriolar damage with microanneyrysms and rupture
What does hypertension do the heart?
Congestive heart failure, atherosclerosis, angina, mI
What does hypertension do the Blood pressure
Persistent elevation
What does hypertension do the Kidneys?
Nephrosclerosis, chronic renal failure
What are the early sins and symptoms in primary hypertension?
Asymptomatic
What are the signs and symptoms of the late stages in primary hypertension?
Fatigue, malaise, headache, blurred vision, nosebleeds
Management/ treatment of primary hypertension?
- Lifestyle modifications, reduce dietary sodiu, weight loss, increase physical activity, decrease dress
- Diuretics, Ace inhibitors
- Other anti hypertensives like beta blockers, alpha 1 blockers, calcium channel blockers
Management/ treatment of secondary hypertension?
Treat cause
All of orthostatic Hypotension: Patho, Cause, S/S Tx
Patho: Lack of vasoconstriction when rising from a supine (laying) positions
Cause decreased blood flow to the brain
Rise slowly to a standing position
Use support when getting up to decrease risk of falls
Post op patients use the fall precautions
Simple: Laying -> standing= Dizzy, decrease in bp
Aging, low blood volume, drug side effects, neutrally mediated hypotension (NHM)
What is arteriosclerosis? what are the results of it?
Generally a term for all types of arterial changes, not just with aging
Elasticity is lost, walls become thick and hard, lumen gradually narrows and may become obstructed= less blood flow because less room for blood to go
This results in diffuse ischemia and necrosis by decreasing blood supply affects kidneys, brain, heart
Atherosclerosis has what? atheromas….?
Differentiated from aterisclosis by the presence of atheromas
Plaque consist of lipid, cells, fibrin, and cell debris, often with attached thrombi, which from inside the walls of large arteries
Where do atheroma usually form?
Large arteries, aorta iliac arteries, coronary arteries, carotid arteries,,,, points f bifurcation
What encourage atheroma development?
Turbulent blood flow
What is the roles of lipids in Atherosclerosis/ CAD?
Low density lipoprotein LDL= bad cholesterol, high lipid content, transport cholesterol from the liver to the cells and leaves deposits through the vessel which leads to atheroma development
High density lipoprotein HDL= low lipid content, transport cholesterol away front he peripheral cells tot he liver where it is broken down Ana’s removed format he body
What is the patho of Atherosclerosis CAD 1-10?
- Endothelial injury of the artery caused by yore tension, smoking, hyperlipidemia, toxiums, viruses, immune reactions
- Endothelial injury»_space; inflammation, cascade
- WBCs and lipids accumulate in the inter lining of muscle layer
- Smooth muscle cells proliferate or multiply
- Plaque forms»_space; more inflammation
- Platelets adhere to touch, damaged surfaces of arterial walls, forming a thrombosis./ clot and partial obstruction (Stacking)
- Lipids and fibrous tissue build up at site of arterial injury
- Platelets adhere and release prostaglandins»_space; more inflammation
- More platelets aggregate at site»_space;> burger thrombus
- Arterial blood becomes more turbulent»_space; thrombus formation continues
Another patho breakdown of Atherosclerosis CAD
Initially atheroma, is a yellow fat streak on the artery wall
Becomes progressively larger, eventually becoming large, firm, projecting mass with an irregular surface on which a thrombus easily forms
Blood flow progressively decrease as the lament narrows
The plaque may ulcerate and break open more inflammation or thrombus resulting in total obstruction = MI
Atheroma dangers the arterial wall weakening the structure decreasing its elasticity eventually calcify causing further rigidity to walls = aneurysm or bulge in wall = rupture and hemorrhage
Complications of atherosclerosis CAD in heart
Partial Occlusion: Angina pectorals ischemic heart disease
Total Occlusion: Myocardial Infarction MI
Complications of atherosclerosis CAD in Brain
Partial Occlusion: Transient ischemic attack
Full Occlusion: Cerebrovascular Accident CVA
Complications of atherosclerosis CAD in peripheral arteries
Aorta: aneurysm, occlusion, rupture and hemorrhage
Legs: Iliac arteries: peripheral vascular disease, gangrene and amputation
What are nonmodifiable factors In atherosclerosis CAD
Age >40
Gender male, females after menopause
Genetic or familial factors
What are modifiable factors in CAD
Obesity: high cholesterol and animal fat, LDL
Sedentary lifestyle
Smoking
Diabetes Melitus
High Cholesterol, hyperlipidemia
Poorly controlled hypertension
How to diagnosis Atherosclerosis CAD?
Exercise stress test
Nuclear medicine studies
Serum lipid levels: HDL and LDL
What is the treatment and lifestyle modifications for Atherosclerosis CAD?
Lose weight, Quit smoking, regular exercise, health diet: low sodium, increase veggies, decrease LDL Trans fat, increase linolenic acid, fish oil, omega three fatty acids
More treatment for atherosclerosis CAD
Lipid reducing drugs Statins
Small does o aspirin to reduce platelet aggregation
Cardiac Catherization and percutaneous trans liminal coronary angioplasty: ROTO ROOTER, stents to keep vessels open
Coronary Artery Bypass grafting CABG Reroute blood flow
What is angina
Myocardial Oxygen supply has fallen below demand
Etiology: Deficit oxygen to heart muscle
CHEST PAIN
Related to impaired blood oxygen or supply or heart: Atherosclerosis, myocardial hypertrophy
Low O2 Level conditions, anemias, respiratory distress
Heart working harder than usual: tachycardia
What is stable Angina?
Doesn’t typically change in frequency and it doesn’t worsen over time
Does not last more than few seconds or minutes
Relieved with nitro
What are predisposing factors for stable angina?
Stress, emotional upset, large meals, rigid exercise, illness, exposure to environmental triggers; weather, pollution
What are manifestations for stable angina?
Recurrent, intermittent brewing episodes of substernal chest pain, diaphoresis, nausea
What is unstable angina?
Blockages in the arteries supplying the hear with blood and oxygen have reached a critical level
Crushing pain occurs at rest or with exertion/ stress
Pain worsens in frequency and severity, not predictable
Signs that a heart attack could occur soon
What is the management for unstable angina?
Nitro
2nd dose of nitro be given if pain persist more than 5 minutes
After 3rd dose within a 101 min period and no pain relief the pain should be treated as a heat attack SEEK CARE ASAP
What are MI, myocardial infarction Manifestations?
Feeling pressure, heaviness, or burning in the chest especially during activity
Sudden substernal chest pain that radiates to left arm, shoulder, jaw or neck
No relief occurs with rest or vasodilators
Silent MI Gastric discomfort more so in women
Sudden shortness of breath, sweating, weakness, fatigue
Nausea ingestion
Anxiety and fear
Hypotension and rapid weak pulse
What are diagnostics for MIs?
ECG Changes
Stemi vs non STEMI, Prolong/ Elvated ST Segment
Labs: TROPINS, most specific for heart tissue damage
Complications of an mI
Sudden death die to dysrhythmias, Vfib, V tach
Cardigenic Shock
HF: Heart Faulyre
Thromboembolism
Management of an MI
MONA:
Morphine- vasodilates
Oxygen- optimization
Nitro- vasodilators
Aspirin- prevents more clots
What is Congestive Heart Failure?
Heart is unable to pump out significant blood to meet metabolic demands of the body
Typically CHF is chronic complication of another condition
Compensatory mechanisms do more harm than good, kidneys
FORWARD effect: cardiac output or stroke volume decreases
- less blood reaching various organs and tissues a forward effects, decreased cell function»_space; fatigue lethargy»_space;> limbs, edema
Beyond the heart not getting enough blood or O2, Cardiac Output, or Stroke volume decreases
Backup effect: Congestion duels in the circulation behind the affected ventricle
Left side: pumps toot the body, gets blood O2 from lungs
Pink frothy sputum= Pulmonary edema
LEFT sided Congestive Heart Failure
Left side of the body pumps oxygenated blood out of the body
If not working fluid will back up to the lungs = Respiratory symptoms
Think COPD, Cough, Shortness of breath, Pulmonary edema
If both LCHR and RCHF usually starts in the left side then develops in right side later
Right Sided Congestive Heart Failure
Right side of the heart pumps deoxygenated blood to the lungs
If not working fluid will back up to the rest of the body= edema!!
Thank systemic edema, fluid overload
Effects of left sided CHF
Decreased CO, Pulmonary congestion AV Stenosis, hyperthyroidism
Orthopnea, can not lay flat, dry or pink frothy sputum, SOB, PND(Can’t breath at night), hemoptysis, RALES
Right Sided Heart Failure Effects
Decreased CO, Systemic congestion and edema of legs and abdomen
Dependent edema in feet, hepatomagly, spelonmegaly, ascites, (abdominal extension), distended neck veins, Flushed face
Diagnosis of CHF
XRAY: Cardiomegaly and fluids
Echocardiogram
ABGs
Cardiac Cath
Management of CHF
Minimize Exersion
Address cause
Avoid fatigue
Vaccine and prevent infection
Reduce workload on heart
Diet: low sodium low carb
Dignoxin
Furosemide
Anti Hypertensives
Diuretics: Lasixs
ACE, ARBS, Caclium channel blockers
Valvular Defects
Stenosis, narrowed valves that restrict blood flow from moving forward
Incompetence Vance does not close completely, allows blood to lack backward
Increase workload reduce efficiency of the heart pump and reduce stroke volume
TX: Susceptible to thrombus formation, anticoagulants and prophylactic antibiotics due to risk of infection of endocarditis
What is rheumatic fever and rheumatic heart disease manifestations and PATHO
Occurs a few weeks after STREP infection
Children 5-15 years
Patho:
Antibodies of strep form and react wit connective tissue in skin, joints, brain, and heart = inflammation
Pericarditis, myocarditis endocarditis affect the valves
Inflammation sites:
Large joints, skin, nodules on wrist, elbows, knees, or ankles
Brain
Scar tissue can form in heart leading to heart disease years later, scarred valves and arrhythmias
More manifestations of Rheumatic fever and heat disease.
Fever 100.8-102
Erythema marginatum, non itchy rash: Bulls eyes red with white center circle rashes
Painful joints
Narrow mitral valve, new murmur
Sydenham chorea, involuntary jerky movements. Of face, arms, and legs = brain
Increase WBCs
Tachycardia even at rest
KEEP BED BOUND
Diagnostic test and manifestations of rheumatic fever and heart disease
Diagnostics: Elevated serum strep antibody levels
Management: penicillin, prolonged period of rest and recovery, anti inflammatory, prophylactic antibiotics before procedure in future
What is infective endocarditis, patho and etiology
Etiology: BACTERIA, hex of valve replacement esp. not medicatied before invasive procedure,
IV Drug users, presses of infection in body, immune compromised
PATHO:
Bacteria - attach to endocardium - inflammation and formation of ventations, nodules, on cusps of the valves
Impaired opening and closing of the valves
Breakaway pieces form infective septic emboli that then causes infarction and infection in other tissues
Manifestations and Management of Endocarditis
Manifestations: New heart murmur, whoosh sound, infection symptoms, loser odes, painful red nodules on the fingers, evidence of septic emboli
Management: antimicrobial drugs for a minimum of 4 weeks, picc line antibiotics, individuals with hex of endocarditis should be premeditated before any invasive procedure with antibiotics.
What is ACUTE Pericarditis, sac around the heart
SECONDARY to any open heart surger, mi’s, rheumatic fever, lupus, etc.
Rough, Swollen surfaces cause chest pain and friction run
Heart can’t expand or contract
Large volumes of fluid in pericardial sac
May compress the heart and impair its expansion and filling, decrease cardiac output= cardiac tap on age
Distended neck veins and faint heart sounds
Pulses paradoxes,, exaggerated drop in systemic bp during inspiration
Pericarditis CHRONIC
Fibrous tissue from TB or radiation to mediastinum
Inflammation of infection may develop from adjacent structures
Results of scar tissue adhesions new teen pericardial membranes
Limits movement of the heart during diastole and systole = reduce cardiac output
S/S: Tachycardia, chest pain, cough, days-near, fatigue, weakness, abdominal discomfort
CARDIAC Tamponade
Manifestations:
Becks triad, muffled heart sounds, hypotension, Jugular vein dissension JVD, Systemic congestion, edema, hepatomegaly
MEDICAL EMERGENCY
Electrical conduction through the heart
SA Node: sinoatrial node 60-100 bpm, pacemaker of the heart
AV node: atrioventricular node 40-60 bpm, backup pacemaker of the heart, delta as impulse passes through here to allow for ventricular filling
AV Bundle: Bundle of his.
Right and left bundle branches
Purkinje fibers 20-40 bpm.
Electrocardiogram ECG/ EKG
Records the electricity activity of the heart
P Wave: atrial depolarizations contraction
QRS Wave: Ventricular activity, Ventricular depolarizations contraction
T Wave: ventricular repolarization relaxation
** you will not see a wave form for atrial relaxation its hidden in the t wave
Cardiac Dysrhythmias/ Arrhythmias
Etiology: damage to normal conduction system of heart
Reduce efficiency of the hearts pumping
Prevents adequate filling
Reduces normal cardiac output
AV Node block, bradycardia, tachycardia, premature atrial contraction (pac), atrial fibrillation, ventricular fibrillation
Tachycardia
Too fast
Sustained HR 100-160 BPM
May be a normal response to sympathetic stimulation, exercise, fever, or stress or it may be compensation for decreased blood volume
Bradycardia SA NODE FIRING
<60bpm
Too slow
Can reduce cardiac output
Often results from vagal nerve or parasympathetic nervous system stimulation
Sick Sinus Sydrome SA NODE FIRING
Alternates between tachycardia and bradycardia
Pacemaker
ATRIAL CONDUCTION
SA nodes s conducting the orchestra multiple impulses from multiple areas of atria
-A Flutter: sawtooth baseline
A Fib: Wavy baseline, irregular rhythm
Turbulent flow and piling in atria - increase risk for clots and stokes
Anticoagulant therapy
Atrial conduction Abnormalities PAC
Premature atrial contractions PACs: Extra contraction or ectopic beats
Atrial form a focus of irritable atrial muscle cells outside the conduction pathway
May feel palpitations
Excessive canine intake, smoking, stress
Arrhythmias Heart blocks
Conduction is excessively delayed or stopped at the AV node or bundle of his
May decrease cardiac output
First Degree at block
Conduction delay, prolongs a PR interval, the time between the atrial and ventricular contractions
Second Degree AV Block
Longer delay leaves periodically to admit, ventricular contraction
Complete or third degree block
No communication between the atria and ventricles
Cardiac output is greatly reduced
May see fainting, syncope
Can lead to heart attack
Premature Ventricular Conduction abnormalities pvc
Premature ventricular contractions PVC
Additional beats from ventricular muscle cell or ectopic pacemaker
Increasing frequency of PVCs multiple ectopic sites or paired beats of concern because ventricular fibrillation can develop from these leading cardiac arrest
Deadly Arrhythmias
V tach: reduce co bc the filling time is reduced and the force of contraction is reduced, may not have a pulse
V Fib: Muscle fibers contract independently and rapidly, ventricles are just quivering and not effecting pumping blood, never a pulse
Pulseless electrical activity PEA: Electrical activity on monitor but heart is not contracting, never a pulse
Asystole: Flat EKG
Arrhythmia Management
Treat underlying cause
Antiarrhythmic drugs, digoxin beta Adrenalin blockers, calcium channel block
CPR
Defibrillators
Cardio version
Pacemaker
Peripheral Vascular Disease
Any abnormalities in the arteries or veins outside the heart
Most common sites of atheromas in the peripheral circulation
Partial occupations may impair both muscle activity and sensory function inn the legs
Total occlusions can lead to necrosis, ulcer, and gangrene
USUALLY IN LEGS
Narrowing lumen
Loss of feeling
Nerve neuropathy
PVD: Peripheral vascular disease signs and symptoms
Increasing fatigue and weakness in legs
Intermittent claudication, leg pain with exercise due to muscle ischemia
Initially pain subsides with rest
As the obstruction advances pain becomes more and more severe and may be present at rest, particularly in the feet and toes
Paraesthesis, tingling, burning, and numbness
1+ Pulse
Color Changes: Pallor or cyanosis when the legs are elevated, rub or or redness when they are dangling
Skin: dry, harmless
Toenails: thick and hard
Feet/ legs: poorly perfumed= feel cold, blue
Treatment of Peripheral vascular disease
Lifestyle: Decrease serum cholesterol, smoking cessation, exercise, dependent leg positions, avoid skin trauma
Medication and Procedures: Peripheral vasodilators, surgical bypass grafts
Aortic Aneurysm
Localized dilation and weakening of an arterial wall
Abdominal or thoracic aorta
Causes: hypertension, atherosclerosis, trauma
Listen for murmur, outing pouching of wall
May rupture= massive bleeding
Aortic aneurysm dx and tx
Frequently asymptomatic for a long period of time until large or rupture
Palpable pulsating abdominal mass with bruit
Rupture or dissection: sever pain, indications for shock, decreased pulses, cool temp
Diagnosis: Radiography Ultrasound, CT, MRI
Treatment: Maintain normal BP, Prevent sudden BP elevations de to exertion stress, coughing, or constipation, surgical repair
Thrombophlebitis and Phlebothrombosis
Blood clot in an inflamed vein
Predisposing factors X3:
1. Stasis is of blood or sluggish blood flow immobility
2. Endothelial injury
3. Increased blood coagulation
Can break off and travel to other area of the body can cause serious problems, PE, Stoke, MI
S/S and TX for thrombophlebitis and phlebothrombosis
S/S: Warmth and redness, arching pain tenderness and edema, positive human sign
Treatment: Compression SCDs or elastic stockings, Exercise, anticoagulation therapy, fibrinolytic therapy
Patho of Shock
Blood pressure determined by blood volume and heart contraction and peripheral resistance
= any decrease - shock
Decrease circulated blood volume = decrease co or generalized massive vasodilation = decrease tissue perfusion = generalized hypoxia
Compensatory mechanism= worse =. Increased vasoconstriction = decreased perfusion = ischemia and necrosis
Hypovolemic shock
low volume
Trauma, hemorrhage, burns, dehydration
Cariogenic shock
Decrease cardiac contractility
MI, PE, Arrhythmia, tamponade, fluid overload
Neurogenic Shock
Loss of sympathetic tone
Spinal cord injury, fear, pain, drugs, hypoglycemia
Anaphylactic Shock
Rapid general vasodilation caused by the release of large amounts of histamine
Severe allergic reaction
Septic Shock
Systemic vasodilation
Severe Infections
Clinical manifestations of shock
1st signs: thirst and agitation and or restlessness
Early signs: vasoconstriction shunts blood from the viscera and skin to the vital areas: cool moist pale skin, tachycardia, tachyons, olguria
Septic Shock warm shock: fever, warm, dry, flushed skin, rapid strong pulse, hyperventilation, evidence of fluid
Later Signs: lethargy weakness, dizziness, weak thready pulses, metabolic acidosis
Shock complications
Renal failure, liver failure, infection, go ischemia, initiation clotting process, multi organ dysfunction ensues, shock becomes irreversible = death
Shock Treatment
Emergency
Supine position, cover and keep warm, O2, Identify cause and reverse
Monitor ABG
Fluids
Antibiotics/ steroids
Vasopressors for BP
