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Pathophysiology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

The circulatory system is composed of

A

Vessels (Arteries,veins,capillaries)
Fluid (Blood , Plasma)
Pump (Heart)

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2
Q

The Heart is located in the

A

mediastinum

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3
Q

The pericardium

A

is a sac that surrounds and protects the heart, helping it function properly

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4
Q

Pericardial cavity

A

The space between parietal & visceral allows room for the heart to increase in size when it fills and to shrink when it contracts

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5
Q

Myocardium

A

Muscle of the heart

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6
Q

Endocardium

A

The inside lining of the heart

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7
Q

Septum

A

Divides the heart between right & left sides

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8
Q

Atrioventricular valves

A

two valves in the heart that control the flow of blood between the atria and ventricles:

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9
Q

Tricuspid valve

A

Located between the right atrium and right ventricle, this valve has three cusps and is anchored to a fibrous ring.

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10
Q

Mitral valve

A

Also known as the bicuspid valve, this valve is located between the left atrium and left ventricle, and has two cusps and a fibrous ring

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11
Q

The semilunar valves

A

are two heart valves that prevent blood from flowing backward into the ventricles from the arteries

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12
Q

Aortic valve

A

Located between the left ventricle and the aorta, this valve ensures that oxygen-rich blood doesn’t flow back into the left ventricle.

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13
Q

Pulmonary valve

A

Located between the right ventricle and the pulmonary artery.

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14
Q

Sinoatrial (SA) node

A

It is the pacemaker of the heart. It is set during embryonic life and it controls rhythm between 60-100 beats per minute.

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15
Q

Atrioventricular (AV) node

A

Second relay(Minor pacemaker which controls the ventricles in the event that the Sinoatrial node does not operate , the AV note will have the ventricles beat between 40-60 beats per minute)

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16
Q

AV bundle(Bundle of His)

A

a bundle of specialized muscle fibers in the heart that carries electrical signals from the atrioventricular (AV) node to the ventricles:

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17
Q

Purkinje fibers

A

are specialized nerve cells that transmit electrical signals to the heart’s ventricles, causing them to contract. This contraction propels blood from the heart to the body’s organs and tissues

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18
Q

Electrocardiogram (ECG)

A

P wave
Depolarization of atria
QRS wave
Depolarization of ventricles(contract)
T wave
Repolarization of ventricles(resting mode)

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19
Q

Medulla oblongata

A

Control center of the heart. Controls rate and force of contraction.

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20
Q

Where are baroreceptors located

A

Medulla oblongata. Located in the aorta and internal carotid arteries.

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21
Q

Baroreceptors

A

Detect changes in blood pressure—sympathetic stimulation(cardiac accelerator nerve, tachycardia). Parasympathetic stimulation(cranial nerve CN X; vagus nerve, bradycardia). Both help maintain heart rate at 60-100 beats per minute.

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22
Q

Factors that increase heart rate

A

1)Thyroid hormones(metabolism).
2)Epinephrine from the sympathetic.
3)Pain
4)Pregnancy
5)Stress response
6)Smoking
7)Exertion or exercise
8)Increased environmental temperature

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23
Q

Right and left coronary arteries(feeds the heart)

A

Blood flows from the left ventricles to the coronary arteries. Branch of aorta immediately distal to the aortic valve.

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24
Q

Left coronary artery divides into

A

Left anterior descending or interventricular artery
Left circumflex artery

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25
Q

Right coronary artery branches

A

Right marginal artery
Posterior interventricular artery

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26
Q

Diastole

A

Relaxation of myocardium required for filling chambers

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27
Q

Systole

A

Contraction of the myocardium provides an increase in pressure to eject blood. The right side of the heart to the lungs. The left side of the heart out the aorta to the body.

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28
Q

The cycle of the heart

A
  1. Right atrium
    Deoxygenated blood enters the heart through the superior vena cava and inferior vena cava, and flows into the right atrium.
  2. Tricuspid valve
    The tricuspid valve opens, allowing blood to flow from the right atrium to the right ventricle.
  3. Right ventricle
    When the right ventricle is full, it contracts and closes the tricuspid valve.
  4. Pulmonary valve
    The pulmonary valve opens, allowing blood to flow from the right ventricle to the pulmonary artery.
  5. Lungs
    Blood travels to the lungs, where it releases carbon dioxide and becomes oxygenated.
  6. Pulmonary veins
    Oxygenated blood returns to the heart through the pulmonary veins and into the left atrium.
  7. Mitral valve
    The mitral valve opens, allowing blood to flow from the left atrium to the left ventricle.
  8. Left ventricle
    When the left ventricle is full, it contracts and closes the mitral valve.
  9. Aortic valve
    The aortic valve opens, allowing blood to flow from the left ventricle to the aorta and the rest of the body.
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29
Q

Heart Sounds

A

“Lubb”—closure of AV valves
“Dub”—closure of semilunar valves
Murmurs(Caused by incompetent valves)
Pulse (Indicates heart rate)
Pulse deficit (Difference in rate between apical and radial pulses). Should be no more than 2 beats. It would indicate the heart is beating , but blood is not moving.

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30
Q

Cardiac output (CO)

A

Blood ejected by a ventricle in 1 minute
CO = SV × HR (heart rate)

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31
Q

Stroke volume (SV)

A

Volume of blood pumped out of ventricle—contraction

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32
Q

Preload

A

Amount of blood delivered to heart by venous return

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33
Q

Afterload

A

Force required to eject blood from ventricles
Determined by peripheral resistance in arteries

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34
Q

Blood Pressure

A

Systolic pressure
Exerted when blood is ejected from ventricles (high)
Diastolic pressure
Sustained pressure when ventricles relax (lower)
Blood pressure (BP) is altered by cardiac output, blood volume, and peripheral resistance to blood flow.

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35
Q

Changes in blood pressure

A

Sympathetic branch of ANS
Increased output → vasoconstriction and increased BP
Decreased output → vasodilation and decreased BP
BP is directly proportional to blood volume.
Hormones
Antidiuretic hormone (↑ BP); aldosterone (↑ blood volume, ↑ BP); renin-angiotensin-aldosterone (vasoconstriction; ↑ BP)

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36
Q

Electrocardiography

A

Electrocardiography- Useful in the initial diagnosis and monitoring of dysrhythmias, myocardial infarction, infection, pericarditis

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37
Q

Auscultation

A

Determination of valvular abnormalities or abnormal shunts of blood that cause murmurs
Detected by listening through a stethoscope

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38
Q

Echocardiography

A

Used to record heart valve movements, blood flow, and cardiac output

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39
Q

Exercise stress tests

A

Used to assess general cardiovascular function

40
Q

Chest x-ray films

A

Used to show shape and size of the heart
Nuclear imaging
Tomographic studies

41
Q

Cardiac catheterization

A

Measures pressure and assesses valve and heart function
Determines central venous pressure and pulmonary capillary wedge pressure

42
Q

Angiography

A

Visualization of blood flow in the coronary arteries

43
Q

Doppler studies

A

Assess blood flow in peripheral vessels
Record sounds of blood flow or obstruction

44
Q

Blood tests

A

Assess levels of serum triglycerides, cholesterol, sodium, potassium, calcium, other electrolytes

45
Q

Arterial blood gas determination

A

Checks the current oxygen level and acid-base balance

46
Q

General Treatment Measures for Cardiac Disorders

A

1)Dietary modifications
To decrease total fat intake
General weight reduction
Reduce salt intake
2)Regular exercise program
Increases high-density lipoprotein levels
Lowers serum lipid levels
Reduces stress levels
3)Cessation of smoking
Decreases risk of coronary disease
4)Vasodilators
Reduction of peripheral resistance
5)Beta blockers
Treatment of hypertension and dysrhythmias
Reduction of angina attacks
6)Calcium channel blockers
Decrease cardiac contractility
Antihypertensives and vasodilators
Prophylactic against angina
7)Digoxin
Treatment for heart failure
Antidysrhythmic drug for atrial dysrhythmias
8)Antihypertensive drugs
Used to lower blood pressure
9)Adrenergic blocking drugs
Act on SNS centrally or on the periphery
10)Angiotensin-converting enzyme (ACE) inhibitors
Block conversion of angiotensin I to angiotensin II
11)Diuretics
Remove excess sodium and/or water.
Treat high BP and congestive heart failure.
12)Anticoagulants
Reduce risk of blood clot formation
13)Cholesterol-lowering drugs
Reduce low-density lipoprotein and cholesterol levels

47
Q

Angina Pectoris

A

Occurs when there is a deficit of oxygen to meet myocardial needs
Chest pain may occur in different patterns.
Classic or exertional angina
Variant angina
Vasospasm occurs at rest.
Unstable angina
Prolonged pain at rest—may precede myocardial infarction

48
Q

Angina Pectoris

A

Recurrent, intermittent brief episodes of substernal chest pain
Triggered by physical or emotional stress
Attacks vary in severity and duration but become more frequent and longer as disease progresses.
Relieved by rest and administration of coronary vasodilators
Example: nitroglycerin
Primarily acts by reducing systemic resistance, decreasing the demand for oxygen

49
Q

Signs and Symptoms Of Angina

A

Pallor
Diaphoresis (excessive sweating)
Nausea

50
Q

Emergency Treatment for Angina

A

Rest, stop activity
Patient seated in upright position
Administration of nitroglycerin—sublingual
Check pulse and respiration.
Administer oxygen, if necessary.
Patient known to have angina
Second dose of nitroglycerin
Patient without history of angina
Emergency medical aid

51
Q

Warnings Signs Of Heart Attack

A

A feeling of pressure , heaviness, or burning in chest-especially with increased activity.
Sudden shortness of breath weakness, fatigue, nausea, Indigestion, Anxiety, and Fear.
Pain may occur and, if present usually (Substernal, Crushing, Radiating)

52
Q

Diagnostic Test

A

Changes in ECG
Serum levels of myosin & (troponin) are elevated within 6 hours
Serum enzyme and isoenzyme levels
Leukocytosis, elevated CRP and ESR common
Arterial blood gas measurements may be altered in severe cases
Pulmonary artery pressure measurements helpful

53
Q

Myocardial Infarction

A

Occurs when coronary artery is totally obstructed
Atherosclerosis is most common cause
Thrombus from atheroma may obstruct artery
Vasospasm is cause in a small percentage.
Size and location of the infarct determine the damage.

54
Q

Type 1 MI(Myocardial Infarction)

A

Type 1 is primarily associated with atherosclerosis and the destruction of cardiac muscle

55
Q

Type 2(Myocardial Infarction)

A

characterized by a mismatch in myocardial oxygen supply

56
Q

Type 3

A

involves only fatal MIs

57
Q

Types 4 & 5

A

are attributed to MIs that occur as a result of a medical procedure(s)

58
Q

Treatment Of Myocardial Infarction

A

Reduce cardiac demand.
Oxygen therapy
Analgesics
Anticoagulants
Thrombolytic agents may be used.
Tissue plasminogen activator
Medication to treat:
Dysrhythmias, hypertension, congestive heart failure
Cardiac rehabilitation begins immediately.

59
Q

Complications Of MI

A

Sudden death
Cardiogenic shock
Congestive heart failure
Rupture of necrotic heart tissue/cardiac tamponade
Thromboembolism causing cerebrovascular accident (CVA; with left ventricular MI)

60
Q

Cardiac Dysrhythmias (Arrhythmias)

A

Deviations from normal cardiac rate or rhythm
Caused by electrolyte abnormalities, fever, hypoxia, stress, infection, drug toxicity
Electrocardiography—for monitoring the conduction system
Detects abnormalities
Reduction of the efficiency of the heart’s pumping cycle
Many types of abnormal conduction patterns exist.

61
Q

Treatment of Cardiac Dysrhythmias (Arrhythmias)

A

Determine cause
i.e. drugs
Change of drug dose might eliminate dysrhythmia
Antiarrhythmic drugs
Beta-adrenergic blockers
Calcium channel blockers
Digoxin
Pacemaker

62
Q

Sinus Node Abnormalities

A

SA node
Pacemaker of the heart; rate can be altered.
Bradycardia
Regular but slow heart rate
Tachycardia
Regular rapid heart rate
Sick sinus syndrome
Marked by altering bradycardia and tachycardia
Often requires mechanical pacemaker

63
Q

Atrial Conduction Abnormalities

A

Premature atrial contractions or beats (PACs, PABs)
Extra contraction or ectopic beats
Irritable atrial muscle cells outside conduction pathway
Atrial flutter
Atrial heart rate of 160 to 350 beats/min
AV node delays conduction—ventricular rate slower
Atrial fibrillation
Rate over 350 beats/min
Causes pooling of blood in the atria
Thrombus formation is a risk.

64
Q

Atrioventricular Node Abnormalities

A

Heart blocks
Conduction excessively delayed or stopped at AV node or bundle of His
First-degree block
Conduction delay between atrial and ventricular contractions
Second-degree block
Every second to third atrial beat dropped at AV node
Third-degree block
No transmission from atria to ventricles

65
Q

Ventricular Conduction Abnormalities

A

Bundle branch block
Interference with conduction in one of the bundle branches
Ventricular tachycardia
Likely to reduce cardiac output as reduced diastole occurs
Ventricular fibrillation
Muscle fibers contract independently and rapidly
Cardiac standstill occurs if not treated immediately!
Premature ventricular contractions (PVCs)
Additional beats from ventricular muscle cell or ectopic pacemaker; may lead to ventricular fibrillation

66
Q

Treatment of Cardiac Dysrhythmias

A

Cause needs to be determined and treated.
Antidysrhythmic drugs are effective in many cases.
SA nodal problems or total heart block require pacemaker
Defibrillator may be implanted for conversion of ventricular fibrillation.

67
Q

Cardiac Arrest

A

Cessation of all heart activity
No conduction of impulses
Flat ECG
Many reasons
Excessive vagal nerve stimulation
Potassium imbalance
Cardiogenic shock
Drug toxicity
Insufficient oxygen
Respiratory arrest
Blow to heart

68
Q

Congestive Heart Failure

A

When heart cannot maintain pumping capability
Cardiac output or stroke volume decreases.
Less blood reaches the various organs.
Decreased cell function
Fatigue and lethargy
Mild acidosis develops.
Backup and congestion develop as coronary demands for oxygen and glucose are not met.
Output from ventricle is less than the inflow of blood.
Congestion in venous circulation draining into the affected side of the heart

69
Q

Backup effects of left-sided failure

A

Related to pulmonary congestion
Dyspnea and orthopnea
Develop as fluid accumulates in the lungs
Cough
Associated with fluid irritating the respiratory passages
Paroxysmal nocturnal dyspnea
Indicates the presence of acute pulmonary edema
Usually develops during sleep
Excess fluid in lungs frequently leads to infections such as pneumonia.

70
Q

Signs of right-sided failure and systemic backup

A

Dependent edema in feet, legs, or buttocks
Increased pressure in jugular veins leads to distention.
Hepatomegaly and splenomegaly
Digestive disturbances
Ascites
Complication when fluid accumulates in peritoneal cavity
Marked abdominal distention
Acute right-sided failure
Flushed face, distended neck veins, headache, visual disturbances

71
Q

Young Children with CHF

A

Often secondary to congenital heart disease
Feeding difficulties often first sign
Failure to gain weight or meet developmental guidelines
Short sleep periods
Tripod position to play
Cough, rapid grunting respirations, flared nostrils, wheezing
Radiographs show cardiomegaly.
Arterial blood gases used to measure hypoxia

72
Q

Congenital Heart Defects

A

cardiac anomalies
Structural defects in the heart that develop during the first 8 weeks of embryonic life
Congenital heart disease
Valvular defects
Septal defects
Detected by the presence of heart murmurs
If untreated, child may develop heart failure.
May be cyanotic or acyanotic, depending on direction of shunting

73
Q

Signs and Symptoms Of Congenital Heart Defects

A

Large defects
Pallor
Tachycardia
Occurs with very rapid sleeping pulse and frequent pulse deficit
Dyspnea on exertion
Squatting position—toddlers and older children
Appears to modify blood flow, more comfortable
Clubbed fingers
Intolerance for exercise and exposure to cold weather
Delayed growth and development

74
Q

Diagnostic Tests Of CHD

A

Severe defects are often diagnosed at birth.
Others may not be detected for some time.
Examination techniques
Radiography
Diagnostic imaging
Cardiac catheterization
Echocardiography
Electrocardiography
Surgical repair

75
Q

Ventricular Septal Defect

A

VSD is the most common congenital heart defect.
Opening in the interventricular septum
May vary in size and location
Untreated VSD
Pressure usually higher in left ventricle.
Shunt from left → right
Acyanotic condition unless respiratory condition increases pressure in right ventricle

76
Q

Treatment Of Ventricular Septal Defect

A

Treatment usually involves both surgical and medical
Surgical
Open heart surgery
Catheter procedure
Hybrid procedure
Medical used to:
Increase strength of contractions
Decrease amount of fluid in circulation
Keep a regular heartbeat.

77
Q

Tetralogy of Fallot

A

Most common cyanotic (R → L shunt) congenital heart condition
Cyanosis occurs because shunt bypasses the pulmonary circulation.
Alters pressures in heart and alters blood flow
Includes four abnormalities
Involves heart as well as joints
VSD
Dextroposition of the aorta
Right ventricular hypertrophy

78
Q

Rheumatic Fever and Rheumatic Heart Disease (1 of 2)

A

Rheumatic fever
Acute systemic inflammatory condition
May result from an abnormal immune reaction
Can occur a few weeks after an untreated infection (usually group A β-hemolytic Streptococcus)
Involves heart as well as joints
Usually occurs in children ages 5 to 15 years
Long-term effects
Rheumatic heart disease
May be complicated by infective endocarditis and heart failure in older adults

79
Q

Rheumatic Fever and Rheumatic Heart Disease (2 of 2)

A

Acute stage—inflammation of the heart
Pericarditis
Myocarditis
Endocarditis and incompetent heart valves
Other sites of inflammation
Large joints
Erythema marginatum
Nontender subcutaneous nodules
Involuntary jerky movement of the face, arms, legs

80
Q

Signs and Symptoms Of Rheumatic Fever & Rheumatic Heart Disease

A

Low-grade fever
Leukocytosis
Malaise
Anorexia, and fatigue
Tachycardia
Heart murmurs
Epistaxis and abdominal pain may be present

81
Q

Infective Endocarditis

A

Subacute
Streptococcus viridans
Acute
Staphylococcus aureus
Basic effects
Same regardless of organism
Factors that predispose to infection
Presence of abnormal valves in heart
Bacteremia
Reduced host defenses

82
Q

Infective Endocarditis (2 of 2)

A

Low-grade fever or fatigue
Anorexia, splenomegaly, congestive heart failure in severe cases
Acute endocarditis
Sudden, marked onset—spiking fever, chills, drowsiness
Subacute endocarditis
Insidious onset—increasing fatigue, anorexia, cough, and dyspnea
Blood culture to identify causative agent
Antimicrobial drugs for several weeks, often IV

83
Q

Pericarditis

A

Usually secondary to another condition
Classified by cause or type of exudate
Acute pericarditis
May involve simple inflammation of the pericardium
May be secondary to:
Open heart surgery, myocardial infarction, rheumatic fever, systemic lupus erythematosus, cancer, renal failure, trauma, viral infection
Effusion may develop.
Large volume of fluid accumulates in pericardial sac
Leads to distended neck veins, faint heart sounds, pulsus paradoxus

84
Q

Chronic pericarditis

A

Results in formation of adhesions between the pericardial membranes
Fibrous tissue often results from tuberculosis or radiation to the mediastinum.
Limiting movement of the heart during diastole and systole → reduced cardiac output
Inflammation or infection may develop from adjacent structures.
Causes fatigue, weakness, abdominal discomfort
Caused by systemic venous congestion

85
Q

Secondary hypertension

A

Results from renal or endocrine disease, pheochromocytoma (benign tumor of the adrenal medulla)
Underlying problem must be treated to reduce blood pressure.

86
Q

Malignant or resistant hypertension

A

Uncontrollable, severe, and rapidly progressive form with many complications
Diastolic pressure is extremely high.

87
Q

Primary Hypertension

A

Essential hypertension
Blood pressure consistently above 140/90 mm Hg
May be adjusted for age
Increase in arteriolar vasoconstriction
Over long period of time—damage to arterial walls
Blood supply to involved area is reduced.
Ischemia and necrosis of tissues, with loss of function

88
Q

Areas most frequently damaged by hypertension

A

Kidneys
Heart
Brain
Retina

89
Q

Predisposing factors To Hypertension

A

Incidence increases with age.
Men affected more frequently and more severely
Incidence in women increases after middle age.
Genetic factors
Sodium intake, excessive alcohol intake, obesity, smoking, prolonged or recurrent stress

90
Q

Hypertension

A

Frequently asymptomatic in early stages
Initial signs vague and nonspecific
Fatigue, malaise, sometimes morning occipital headache
Essential hypertension treated in steps
Lifestyle changes
Reduction of sodium intake
Weight reduction
Reduction of stress
Drugs
Diuretics, ACE inhibitors, drug combinations

91
Q

Shock

A

Hypovolemic shock
Loss of circulating blood volume
Cardiogenic shock
Inability of heart to maintain cardiac output to circulation
Distributive, vasogenic, neurogenic, septic, anaphylactic shock
Changes in peripheral resistance leading to pooling of blood in the periphery

92
Q

Shock: Early Manifestations

A

Anxiety
Tachycardia
Pallor
Light-headedness
Syncope
Sweating
Oliguria

93
Q

Compensation mechanisms Of Shock

A

SNS and adrenal medulla stimulated—increase heart rate, force of contraction, systemic vasoconstriction
Renin secretion increases.
Increased ADH secretion
Secretion of glucocorticoids
Acidosis stimulates increased respiration.
With prolonged shock, cell metabolism is diminished, waste not removed—leads to lower pH

94
Q

Complications of shock

A

Acute renal failure
Shock lung, or adult respiratory distress syndrome
Hepatic failure
Paralytic ileus, stress or hemorrhagic ulcers
Infection or septicemia
Disseminated intravascular coagulation
Depression of cardiac function

95
Q

Phlebothrombosis

A

formation of a blood clot in a vein that is not inflamed.

96
Q
A

Pathophysiology (7 decks)

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