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Pathophysiology Taylor > Exam #2: Cardiac > Flashcards

Exam #2: Cardiac Flashcards

1
Q

What are the 4 common cardiac diagnostic test, and what does each do?

A
  1. EKG/ ECG: Electrocardiogram: Conduct electrical activity of the heart
  2. Echocardiogram Ultrasound of the heart: Changes in heart structure of function, valve, congenital
  3. Stress Test: checking for exercise induced problems such as arrhythmias
  4. Cardiac Catheterization: Visualize the inside of the coronary arteries look for blocked arteries and clear them out to restore blood flow
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2
Q

What is hypertension and when does it occur, what effects it?

A

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

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3
Q

What are we seeing in teenagers right now?

A

Hypertension, Type 2 Diabetes, Bad Diet, Poor Lifestyle choices

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4
Q

Cardiomeagly

A

Enlarged heart because it. Is working harder

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5
Q

What are the three major categories of hypertension?

A

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

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6
Q

Why do we care if one has hypertension?

A

Straining on the heart

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7
Q

Pathophysiology of Primary hypertension

A

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

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8
Q

What does hypertension do the brain?

A

Cerebral aneurysm hemorrhagic CVA Stoke

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9
Q

What does hypertension do the eyes?

A

Retinopathy, arteriolar damage with microanneyrysms and rupture

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10
Q

What does hypertension do the heart?

A

Congestive heart failure, atherosclerosis, angina, mI

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11
Q

What does hypertension do the Blood pressure

A

Persistent elevation

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12
Q

What does hypertension do the Kidneys?

A

Nephrosclerosis, chronic renal failure

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13
Q

What are the early sins and symptoms in primary hypertension?

A

Asymptomatic

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14
Q

What are the signs and symptoms of the late stages in primary hypertension?

A

Fatigue, malaise, headache, blurred vision, nosebleeds

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15
Q

Management/ treatment of primary hypertension?

A
  1. Lifestyle modifications, reduce dietary sodiu, weight loss, increase physical activity, decrease dress
  2. Diuretics, Ace inhibitors
  3. Other anti hypertensives like beta blockers, alpha 1 blockers, calcium channel blockers
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16
Q

Management/ treatment of secondary hypertension?

A

Treat cause

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17
Q

All of orthostatic Hypotension: Patho, Cause, S/S Tx

A

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)

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18
Q

What is arteriosclerosis? what are the results of it?

A

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

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19
Q

Atherosclerosis has what? atheromas….?

A

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

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20
Q

Where do atheroma usually form?

A

Large arteries, aorta iliac arteries, coronary arteries, carotid arteries,,,, points f bifurcation

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21
Q

What encourage atheroma development?

A

Turbulent blood flow

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22
Q

What is the roles of lipids in Atherosclerosis/ CAD?

A

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

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23
Q

What is the patho of Atherosclerosis CAD 1-10?

A
  1. Endothelial injury of the artery caused by yore tension, smoking, hyperlipidemia, toxiums, viruses, immune reactions
  2. Endothelial injury&raquo_space; inflammation, cascade
  3. WBCs and lipids accumulate in the inter lining of muscle layer
  4. Smooth muscle cells proliferate or multiply
  5. Plaque forms&raquo_space; more inflammation
  6. Platelets adhere to touch, damaged surfaces of arterial walls, forming a thrombosis./ clot and partial obstruction (Stacking)
  7. Lipids and fibrous tissue build up at site of arterial injury
  8. Platelets adhere and release prostaglandins&raquo_space; more inflammation
  9. More platelets aggregate at site&raquo_space;> burger thrombus
  10. Arterial blood becomes more turbulent&raquo_space; thrombus formation continues
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24
Q

Another patho breakdown of Atherosclerosis CAD

A

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

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25
Q

Complications of atherosclerosis CAD in heart

A

Partial Occlusion: Angina pectorals ischemic heart disease

Total Occlusion: Myocardial Infarction MI

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26
Q

Complications of atherosclerosis CAD in Brain

A

Partial Occlusion: Transient ischemic attack

Full Occlusion: Cerebrovascular Accident CVA

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27
Q

Complications of atherosclerosis CAD in peripheral arteries

A

Aorta: aneurysm, occlusion, rupture and hemorrhage

Legs: Iliac arteries: peripheral vascular disease, gangrene and amputation

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28
Q

What are nonmodifiable factors In atherosclerosis CAD

A

Age >40
Gender male, females after menopause
Genetic or familial factors

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29
Q

What are modifiable factors in CAD

A

Obesity: high cholesterol and animal fat, LDL
Sedentary lifestyle
Smoking
Diabetes Melitus
High Cholesterol, hyperlipidemia
Poorly controlled hypertension

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30
Q

How to diagnosis Atherosclerosis CAD?

A

Exercise stress test
Nuclear medicine studies
Serum lipid levels: HDL and LDL

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31
Q

What is the treatment and lifestyle modifications for Atherosclerosis CAD?

A

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

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32
Q

More treatment for atherosclerosis CAD

A

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

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33
Q

What is angina

A

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

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34
Q

What is stable Angina?

A

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

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35
Q

What are predisposing factors for stable angina?

A

Stress, emotional upset, large meals, rigid exercise, illness, exposure to environmental triggers; weather, pollution

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36
Q

What are manifestations for stable angina?

A

Recurrent, intermittent brewing episodes of substernal chest pain, diaphoresis, nausea

37
Q

What is unstable angina?

A

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

38
Q

What is the management for unstable angina?

A

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

39
Q

What are MI, myocardial infarction Manifestations?

A

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

40
Q

What are diagnostics for MIs?

A

ECG Changes
Stemi vs non STEMI, Prolong/ Elvated ST Segment

Labs: TROPINS, most specific for heart tissue damage

41
Q

Complications of an mI

A

Sudden death die to dysrhythmias, Vfib, V tach
Cardigenic Shock
HF: Heart Faulyre
Thromboembolism

42
Q

Management of an MI

A

MONA:
Morphine- vasodilates
Oxygen- optimization
Nitro- vasodilators
Aspirin- prevents more clots

43
Q

What is Congestive Heart Failure?

A

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&raquo_space; fatigue lethargy&raquo_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

44
Q

LEFT sided Congestive Heart Failure

A

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

45
Q

Right Sided Congestive Heart Failure

A

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

46
Q

Effects of left sided CHF

A

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

47
Q

Right Sided Heart Failure Effects

A

Decreased CO, Systemic congestion and edema of legs and abdomen

Dependent edema in feet, hepatomagly, spelonmegaly, ascites, (abdominal extension), distended neck veins, Flushed face

48
Q

Diagnosis of CHF

A

XRAY: Cardiomegaly and fluids

Echocardiogram
ABGs
Cardiac Cath

49
Q

Management of CHF

A

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

50
Q

Valvular Defects

A

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

51
Q

What is rheumatic fever and rheumatic heart disease manifestations and PATHO

A

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

52
Q

More manifestations of Rheumatic fever and heat disease.

A

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

53
Q

Diagnostic test and manifestations of rheumatic fever and heart disease

A

Diagnostics: Elevated serum strep antibody levels

Management: penicillin, prolonged period of rest and recovery, anti inflammatory, prophylactic antibiotics before procedure in future

54
Q

What is infective endocarditis, patho and etiology

A

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

55
Q

Manifestations and Management of Endocarditis

A

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.

56
Q

What is ACUTE Pericarditis, sac around the heart

A

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

57
Q

Pericarditis CHRONIC

A

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

58
Q

CARDIAC Tamponade

A

Manifestations:
Becks triad, muffled heart sounds, hypotension, Jugular vein dissension JVD, Systemic congestion, edema, hepatomegaly

MEDICAL EMERGENCY

59
Q

Electrical conduction through the heart

A

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.

60
Q

Electrocardiogram ECG/ EKG

A

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

61
Q

Cardiac Dysrhythmias/ Arrhythmias

A

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

62
Q

Tachycardia

A

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

63
Q

Bradycardia SA NODE FIRING

A

<60bpm
Too slow
Can reduce cardiac output
Often results from vagal nerve or parasympathetic nervous system stimulation

64
Q

Sick Sinus Sydrome SA NODE FIRING

A

Alternates between tachycardia and bradycardia
Pacemaker

65
Q

ATRIAL CONDUCTION

A

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

66
Q

Atrial conduction Abnormalities PAC

A

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

67
Q

Arrhythmias Heart blocks

A

Conduction is excessively delayed or stopped at the AV node or bundle of his

May decrease cardiac output

68
Q

First Degree at block

A

Conduction delay, prolongs a PR interval, the time between the atrial and ventricular contractions

69
Q

Second Degree AV Block

A

Longer delay leaves periodically to admit, ventricular contraction

70
Q

Complete or third degree block

A

No communication between the atria and ventricles
Cardiac output is greatly reduced
May see fainting, syncope
Can lead to heart attack

71
Q

Premature Ventricular Conduction abnormalities pvc

A

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

72
Q

Deadly Arrhythmias

A

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

73
Q

Arrhythmia Management

A

Treat underlying cause
Antiarrhythmic drugs, digoxin beta Adrenalin blockers, calcium channel block
CPR
Defibrillators
Cardio version
Pacemaker

74
Q

Peripheral Vascular Disease

A

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

75
Q

PVD: Peripheral vascular disease signs and symptoms

A

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

76
Q

Treatment of Peripheral vascular disease

A

Lifestyle: Decrease serum cholesterol, smoking cessation, exercise, dependent leg positions, avoid skin trauma

Medication and Procedures: Peripheral vasodilators, surgical bypass grafts

77
Q

Aortic Aneurysm

A

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

78
Q

Aortic aneurysm dx and tx

A

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

79
Q

Thrombophlebitis and Phlebothrombosis

A

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

80
Q

S/S and TX for thrombophlebitis and phlebothrombosis

A

S/S: Warmth and redness, arching pain tenderness and edema, positive human sign

Treatment: Compression SCDs or elastic stockings, Exercise, anticoagulation therapy, fibrinolytic therapy

81
Q

Patho of Shock

A

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

82
Q

Hypovolemic shock

A

low volume
Trauma, hemorrhage, burns, dehydration

83
Q

Cariogenic shock

A

Decrease cardiac contractility
MI, PE, Arrhythmia, tamponade, fluid overload

84
Q

Neurogenic Shock

A

Loss of sympathetic tone
Spinal cord injury, fear, pain, drugs, hypoglycemia

85
Q

Anaphylactic Shock

A

Rapid general vasodilation caused by the release of large amounts of histamine
Severe allergic reaction

86
Q

Septic Shock

A

Systemic vasodilation

Severe Infections

87
Q

Clinical manifestations of shock

A

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

88
Q

Shock complications

A

Renal failure, liver failure, infection, go ischemia, initiation clotting process, multi organ dysfunction ensues, shock becomes irreversible = death

89
Q

Shock Treatment

A

Emergency
Supine position, cover and keep warm, O2, Identify cause and reverse

Monitor ABG
Fluids
Antibiotics/ steroids
Vasopressors for BP

Pathophysiology Taylor (5 decks)

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