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Adv Patho > Cardiovascular_Exam 2: Ch. 33, 34 > Flashcards

Cardiovascular_Exam 2: Ch. 33, 34 Flashcards

1
Q

What factors contribute to blood flow in a vessel

A
  1. compliance
  2. pressure and resistance
  3. velocity
  4. turbulent vs. laminar flow
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2
Q

Which coronary arteries provide blood to which part of the heart?

A

Right coronary artery supplies blood to right atrium, right ventricle, SA node, and AV node

Left coronary artery supplies blood to left atrium, left ventricle, and interventricular septum

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3
Q

What does Qp : Qs mean and what factors alter a normal ratio?

A

ratio to pulmonary to systemic flow, describes the magnitude of a vascular shunt

Qp=pulmonary flow
Qs=systemic flow

Normally=1:1. left to right shunts>1.0; right to left shunts Qp/Qs <1

A cardiac shunt is a pattern of blood flow in the heart that deviates from the normal circuit of the circulatory system

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4
Q

Catecholamine effect on cardiovascular system

A

Increase heart rate, bp, breathing rate, muscle strength, and mental alertness

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5
Q

Epinephrine effect on cardiovascular system

A

Increases heart rate. Vasoconstriction in most systemic arteries and veins. INCREASED CARDIAC OUTPUT and redistribution of the cardiac output to muscular and hepatic circulation with only a small change in the arterial pressure

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6
Q

Norepinephrine effect on cardiovascular system

A

Increase in heart rate and inotropy.
Vasoconstriction occus in most systemic arteries and veins.
INCREASED CARDIAC OUTPUT and SYSTEMIC VASCULAR RESISTANCE which results in an ELEVATION IN ARTERIAL BLOOD PRESSURE

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7
Q

Dopamine effect on cardiovascular system

A

increased pulse pressure, heart rate, and circulating epinepherine and norepinepherine levels

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8
Q

ACUTE CORONARY SYNDROME -STEMI

A

DEFINITION: ST elevation; continued coronary occlusion which leads to transmural infarction extending from endocardium to pericardium. Leads to myocyte necrosis and death.

CLINICAL MANIFESTATIONS: sudden severe chest pain that is prolonged. “Elephant sitting on chest”. Radiates to neck, jaw, back, shoulder, or left arm is common.

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9
Q

ACUTE CORONARY SYNDROME -UNSTABLE ANGINA (PRINZMETAL)

A

DEFINITION: type of acute CAD that results in reversible myocardial ischemia

CLINICAL MANIFESTATIONS: new onset angina, angina that occurs at rest, or angina that is increasing in severity or frequency. May also experience dyspnea, diaphoresis, and anxiety as it gets worse.

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10
Q

Evaluate the differences in the extent of an infarction of the myocardium secondary to an NSTEMI and a STEMI (these are 2 types of myocardial infarctions)

A

NSTEMI: ST depression and T-wave inversion. Thrombus is less liable and occludes the vessel for a prolonged period that leads to myocardial ischemia and leads to myocyte necrosis and death. Thrombus will break up before complete distal tissue necrosis and only myocardium directly under endocardium will be involved.

STEMI: ST elevation. When thrombus lodges permanently in vessel, the infarction will extend through the myocardium all the way to the endocardium or epicardium resulting in severe cardiac dysfunction.

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11
Q 
Preload definition
(also end diastolic volume)
A

amount of blood in ventricle at the end of atrial systole just prior to ventricular contraction

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12
Q

Afterload definition

A

resistance to ejection of blood from the left ventricle

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13
Q

Stroke volume definition

A

the amount of blood pumped of by a ventricle with each beat

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14
Q

End systolic volume definition

A

the volume of blood in the left or right ventricle at the end of the systolic ejection phase immediately before the beginning of diastole or ventricular filling

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15
Q

Ejection Fraction definition

A

a measurement % of how much blood the ventricle pumps out with each contraction

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16
Q

Cardiac output definition

A

the amount of blood the heart pumps through the circulatory system in a minute

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17
Q

A Fib causes

A

in atrial fibrillation, the signals in the upper chambers of the heart are chaotic. As a result, the upper chambers shake (quiver). The AV node is then bombarded with signals trying to get through to the lower heart chambers (ventricles). This causes a fast and irregular heart rhythm.

**100-175 bpm

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18
Q

A Fib risk factors

A 
Advancing age
High BP
obesity
European ancestory
Diabetes
heart failure
ischemic heart disease
hyperthyroidism
CKD
moderate to heavy alcohol use
Smoking
Englargement of chambers on the left side of the heart
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19
Q

A Fib Pathophysiology**

A

hypertension, structural, valvular, and ischemic heart disease illicit the paroxysmal and persistent forms of atrial fibrillation

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20
Q

A Fib Manifestions

A

palpitations, dizziness, CP, fainting, dyspnea, pallor, fatigue, nervousness, cyanosis

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21
Q

PVC causes

A

are extra heartbeats that begin in one of your heart’s two lower pumping chambers (ventricles). These extra beats disrupt your regular heart rhythm, sometimes causing you to feel a fluttering or a skipped beat in your chest.

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22
Q

PVC risk factors

A

caffeine, tobacco, drugs, exercise, high BP, anxiety, heart disease

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23
Q

What does pulmonary circulation do?

A

movingbloodbetweentheheartandthelungs.Ittransports deoxygenatedbloodtothelungstoabsorboxygenandreleasecarbondioxide.

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24
Q

PVC manifestations

A

palpitations, dizzy, anxiety

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25
Q

What is the role of lipoproteins?

A

Lipoproteins provide a transport for lipids, phospholipids, cholesterol, and triglycerides as described below. … Transport of cholesterol to organs and tissues; cholesterol is required for the formation of membranes of red blood cells and for the production of steroid hormones. In the liver it is converted to bile acids.

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26
Q

How do the lipoproteins inform your knowledge of a persons cardiovascular risk?

Very-low-density lipoproteins (triglycerides)

A

may contribute to hardening of the arteries or thickening of the artery walls (arteriosclerosis) — which increases the risk of stroke, heart attack and heart disease.

Normal <150

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27
Q

How do the lipoproteins inform your knowledge of a persons cardiovascular risk?

Low-density lipoproteins (LDL)

A

positive association with atherosclerosis; cholesterol

increased levels indicator of risk of CAD
Normal: <100

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28
Q

How do the lipoproteins inform your knowledge of a persons cardiovascular risk?

High-density lipoproteins (HDL)

A

-negative association with atherosclerosis; phospholipids
-referred to as the “good” cholesterol because it helps remove other, more harmful forms of cholesterol from your blood.
Normal >40

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29
Q

What are the risk factors for dyslipidemia?

A

Genetics, obesity, unhealthy diet, lack of exercise

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30
Q

Describe the progression of atherosclerosis.

A
  1. damaged endothelium
  2. fatty streak and lipid core formation
  3. fibrous plaque formation
  4. complicated lesion, possible rupture
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31
Q

What is peripheral artery disease and how does it manifest?

A

-common circulatory problem in which narrowed arteries reduce blood flow to the limbs, cause by atherosclerosis, smoking, drug use, etc

Manifestations:
Pain and tenderness of the affected part
Painful cramping in one or both of the hips thighs or calf muscles after certain activities such as walking or climbing stairs (claudication)
Leg numbness/weakness
Coldness in the lower leg or foot, especially when compared with the other side
Sore on the toes, feet or legs that won’t heal

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32
Q

What factors contribute to determining a blood pressure?

A
  1. cardiac output
  2. peripheral vascular resistance
  3. volume of circulating blood
  4. viscosity of blood
  5. elasticity of blood vessel walls
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33
Q

What is hypertension and what are common causes?

A

-increased cardiac output, increased peripheral resistance
-sustained elevation >140/90 adults
Risk factors: genetics, age, gender and race, environment, dietary

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34
Q

What is compliance

A

vascular compliance is the increase in volume a vessel is able to accommodate for a given increase in pressure. Compliance is an index of the elasticity of the vessel. Stiffness is the opposite of compliance.

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35
Q

What can cause increase in blood viscosity?

A

increase in red cell content, increased plasma levels of fibrinogen and coagluation factors, and dehydration

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36
Q

Discuss how electrolyte imbalances affect conduction, contraction or resistance with POTASSIUM

A
  • Contributes to repolarization phase of the action potential
  • *Hyperkalaemia can cause suppressed conduction, resulting in tall, peaked T waves, or a prolonged PR interval and a widened QRS interval, Cardiac arrest from complete heart block at much higher K.
  • *Hypokalaemia, decreased membrane excitability. A typical ECG for a patient with hypokalaemia will show flattened T waves, U waves (waves following a T wave, not typically seen on standard ECG traces), depressed ST segments or premature ventricular or atrial complexes that may signal worsening conduction blockade; at the extreme it can indicate impending ventricular tachycardia.
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37
Q

Discuss how electrolyte imbalances affect conduction, contraction or resistance CALCIUM

A

-Contributes to cardiac and smooth muscle contraction

**Myocardial contractility may initially increase until the calcium level reaches >15 mg/dL. Above this level myocardial depression occurs. Hypercalcemia may cause hypertension. Many patients with hypercalcemia develop hypokalemia. Both of these conditions contribute to cardiac arrhythmias.

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38
Q

Discuss how electrolyte imbalances affect conduction, contraction or resistance MAGNESIUM

A

-Interacts with calcium, contributes to myocardial metabolism, improved vascular smooth muscle tone and peripheral vascular resistance, after load, and cardiac output

  • Hypomagnesemia can cause arrhythmia; prolongation of conduction and slight ST depression
  • Hypermagnesemia can cause hypotension; depresses conduction system
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39
Q

What does troponin lab tell us?

A

Not normally found in the blood. When heart muscle gets damaged, troponin is released into bloodstream.

40
Q

Where does cardiac impulse orginate?

A

SA node

41
Q

Cardiac conduction pathway

A

Impulse sent to SA node»RA»LA»av node»bundle of HIS»purkinje fibers»gap junctions

42
Q

Describe those persons most at risk for, the etiology of, and the presentation (clinical manifestations) different types of myocardial ischemia-STABLE ANGINA

A

ETIOLOGY: caused by gradual luminal narrowing and hardening of the arterial walls. It occurs in exercise or under emotional stress. If the demand drops, no necrosis of myocardial cells results. With rest, blood flow is restored and no necrosis of MI cells

RISK FACTORS: obese, smoking, high cholesterol, high bp, no exercise

MANIFESTATIONS: chest pain, pain may radiate to the neck, lower jaw, left arm, and left shoulder, or back or down the right arm

43
Q

Describe those persons most at risk for, the etiology of, and the presentation (clinical manifestations) different types of myocardial ischemia-UNSTABLE ANGINA aka PRINZMETAL ANGINA

A

ETIOLOGY: characterized by recurrent episodes of chest pain that usually occur when a person is at rest, between midnight and early morning.

RISK FACTORS: obese, smoking, high cholesterol, high bp, no exercise, diabetes, family hx, males

MANIFESTATIONS: chest pain that is due to transient ischemia of the myocardium; usually benign. CP occurs at rest

44
Q

Describe those persons most at risk for, the etiology of, and the presentation (clinical manifestations) different types of myocardial ischemia-SILENT ISCHEMIA

A

ETIOLOGY: no feeling of chest pain. Non‐specific symptoms, atypical, such as fatigue, a feeling of unease. Common in woman. Silent ischemia may occurs during mental distress.

RISK FACTORS: diabetes, recent heart attack, unmanaged stress, older age, high bp, obese, high cholesterol, tobacco, sedentary lifestyle

MANIFESTATIONS: fatigue, dyspnea, or feeling of unease

45
Q

Symptoms and Risk factors for CAD

A

Symptoms: angina, weakness, pain in arms or shoulders, SOB

Risk factors: high BP, dyslipidemia, smoking, insulin resistance, obese, inactivity, hx of preeclampsia during pregnancy, stress, inactivity, unhealthy eating habits

46
Q

Diagnosis of CAD and treatement

A

Dx: EKG, echocardiogram, stress test , cardiac catheterization (left heart cath), heart CT scan

Treatment: angioplasty and stent placement, coronary artery bypass graft surgery; enhanced external counterpulsation

47
Q

This is the key lab used in diagnosing a myocardial infarct ________________. Other labs that may be useful in patients who have an MI include and why?

A

***Troponin; serial troponins

  • CPK-MB and LDH are biomarkers released by myocardial cells
  • elevated CRP, leukocytosis=inflammation

-12 lead EKG will show ST elevation and a Q wave some hours later

48
Q

Differentiate between left-sided and right-sided heart failure.

LEFT SIDED HF (aka CHF)

A

ETIOLOGY: HF with reduced ejection fraction (systolic HF) or preserved ejection fraction (diastolic HF). EF <40%. 50% of cases of HF

RISK FACTORS: genetics, age, smoking, obesity, diabetes, renal failure, valvular heart disease, cardiomyopathies, myocarditis, congenital heart disease, excessive alcohol

CLINICAL MANIFESTATIONS: dyspnea, orthopnea, cough with frothy sputum, fatigue, decrease urine output, and edema. Physical exam will show pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension, hypertension, and S3 gallop, and evidence of underlying CAD or HTN

PATHO: decreased compliance and abnormal diastolic relaxation

49
Q

Differentiate between left-sided and right-sided heart failure.

RIGHT SIDE HF (aka cor pulmonale)

A

ETIOLOGY: failure of right ventricle to provide circulation to pulmonary circulation. Generally result of left sided heat failure and increased resistance for right ventricle to over come. Blood backs up into venous circulation. If no left sided HE, consider pulmonary hypertension

RISK FACTORS: Left side HF, RV ventricular MI, cardiomyopathies, and pulmonic valvular disease

CLINICAL MANIFESTATIONS: sob, dizzy, CP, swelling of feet, fainting spells, chest discomfort

PATHO: if not due to Left HF it can be due to high blood pressure in the arteries of the lungs known as called pulmonary hypertension.

50
Q

Name 3 types of myocardial ischemia (MI)

A
  1. Stable Angina
  2. Unstable angina (Prinzmetal)
  3. Silent Ischemia
51
Q

Endocarditis

A

ETIOLOGY: infective (esp. strep and staph); affect valves

RISK FACTORS: age, artificial valves, damage heart valves, congenital heart disease, hx drugs, bad teeth, hx endocarditis

CLINICAL MANIFESTATIONS: new or change heart murmur, SOB, night sweats, swelling feet, legs, or abd, fatigue, flu-like symptoms, achy joints/muscles, chest pain with breathing

PATHO: endocardial damage, microorganisms adhere to the endocardial surface, adherent bacteria form vegetative lesions on valve surfaces

52
Q

Explain the process of ventricular remodeling.

A

changes in left ventricular (LV) geometry, mass, and volume in response to myocardial injury or alterations in load. When contractility is decreased, stroke volume falls, and left ventricular end diastolic volume increase. This causes dilation of heart and increase preload. The extent of LV dilatation or remodeling after myocardial infarction (MI) or in patients with heart failure is a strong predictor of both morbidity and mortality.

53
Q

Explain ventricular remodeling

A

refers to changes in the size, shape, structure, and function of the heart. This can happen as a result of exercise (physiological remodeling) or after injury to the heart muscle (pathological remodeling)

54
Q

What can cause increase in blood viscosity?

A

increase in red cell content, increased plasma levels of fibrinogen and coagulation factors, and dehydration

55
Q

Causes of pericarditis and symptoms

A
  • idiopathic, viral, connective tissue disease
    symptoms: fever, malaise, chest pain, friction rub–most common is stabbing CP that may ravel to the left shoulder and neck. Sudden and doesn’t last long.
  • may results in pericardial effusion
56
Q

Types of Transient ischemia

A

stable angina, prinzmetal angina, and silent ischema

process of atherosclerotic plaque progression can be gradual which results in transient MI syndromes when demand for blood supply exceeds supply, but perfusion is restored before there is damage to the heart muscle

57
Q

Explain the process of cardiac contraction and relaxation (role of actin, myosin and troponin).

A

The cardiac cycle refers to the alternating contraction and relaxation of the myocardium in the walls of the heart chambers, coordinated by the conduction system, during one heartbeat.
ACTIN- The actin filaments slide past the myosin filaments toward the middle of the sarcomere. The result is shortening of the sarcomere without any change in filament length.

MYOSIN -moves its head groups along the actin filament in the direction of the plus end. This movement slides the actin filaments from both sides of the sarcomere toward the M line, shortening the sarcomere and resulting in muscle contraction.

TROPONIN- calcium binds to troponin which enable the cross bridge muscle contraction

58
Q

What is the conduction pathway?

A

**each time your heart beats, electrical signals that controls your heart beat

**Pathway: Impulse starts at SA node&raquo_space; action potential spreads throughout right and left atria&raquo_space; impulse passes from atria into ventricles through AV node&raquo_space; action potential is briefly delayed at AV node&raquo_space; impulse travels rapidly down interventricular septum by means of bundle of His&raquo_space; impulse rapidly disperses throughout myocardium by means of purkinje fibers&raquo_space; rest of ventricular cells activated by cell to cell spread of impulse through gap junctions

59
Q

How does conduction correlate with the EKG and activity in the heart?

A

During a cardiac cycle a wave of depolarization passes from the atrial pacemaker cells over the atrium and down the AV bundle to spread through the ventricular myocardial syncytium.

60
Q

Describe acute and chronic complications of hypertension.

A

Acute: exacerbation of pre-existing HTN; aka severe spike in bp that could end in organ damage. AKA hypertensive emergency

Chronic HTN can lead to complicated HTN if not treated: retinal changes, renal disease, cardiac disease, neurologic disease

61
Q

Pulmonary Circulation

A

moving blood between the heart and the lungs. It transports deoxygenated blood to the lungs to absorb oxygen and release carbon dioxide.

62
Q

Systemic circulation

A

moving blood between the heart and the rest of the body. It sends oxygenated blood out to cells and returns deoxygenated blood to the heart.

63
Q

Blood flow

A

1 . The blood first enters the right atrium.

  1. The blood then flows through the tricuspid valve into the right ventricle.
  2. When the heart beats, the ventricle pushes blood through the pulmonic valve into the pulmonary artery.
  3. The pulmonary artery carries blood to the lungs where it “picks up” oxygen and then leaves the lungs to return to the heart through the pulmonary vein.
  4. The blood enters the left atrium, then descends through the mitral valve into the left ventricle.
  5. The left ventricle then pumps blood through the aortic valve and into the aorta, the artery that feeds the rest of the body through a system of blood vessels.
  6. Blood returns to the heart from the body via two large blood vessels called the superior vena cava and the inferior vena cava. This blood carries little oxygen, as it is returning from the body where oxygen was used.
  7. The vena cavas pump blood into the right atrium and the cycle of oxygenation and transport begins all over again.
64
Q

ST interval

A

time when ventricular fibers are fully depolarized

65
Q

TP interval

A

when the heart muscle is completely at rest and ventricular filling is taking place

66
Q

P wave

A

depolarization

67
Q

what is known as the pacemaker of the heart

A

SA node

68
Q

Discuss how electrolyte imbalances affect conduction, contraction or resistance with SODIUM**

A
  • Participates in maintaining cell membrane potential, also influences serum osmolality
  • can cause increased heart rate, elevated blood pressure and fluid retention, etc. Hyponatremia/hyper both can be accompanied by volume depletion –low BP, tachycardia; volume expansion –edema, ascites…
69
Q

QRS complex

A

ventricular depolarization (atria repolarization simultaneously)

70
Q

T wave

A

ventricular repolarization

71
Q

PR interval

A

conduction time from the end of atrial depolarization to the onset of ventricular depolarization

72
Q

In heart failure, preload is chronically _______

A

elevated

73
Q

In HTN, afterload is chronically ___________

A

elevated

74
Q

Qp/Qs ratio for:*****p.1124

  1. ventricular septal defect ( left to right shunt)
  2. patent ductus arteriosus
  3. atrial septal defect
  4. patent foramen ovale
A
  1. > 2:1
  2. > 2
  3. > 1
  4. > 1.5
75
Q

Diastolic

A

Atria and ventricles are relaxed. The chambers fill with blood.
Bottom number

76
Q

Systolic

A

period of time when heart muscle is contracting

Top number

77
Q

Primary HTN

A

result of genetics and environment that increases vascular tone (increased peripheral resistance) and blood volume.

78
Q

Secondary HTN

A

caused by underlying disease process that raises peripheral vascular resistance or cardiac output. Ex: renal disease, adrenocortical tumors, drugs. BP can return to norm if cause is identified and removed before permanent damage occurs

79
Q

Complicated HTN

A

chronic HTN that damages walls of systemic blood vessels. Complications: angina pectoris, LV hypertrophy lead to CHF, CAD, MI, and sudden death.

80
Q

What is the sympathetic nervous system role in hypertension?

A

SNS contributes to the pathogenesis of HTN. It maintains adequate blood pressure and tissue perfusion by promoting cardiac contractility and heart rate by inducing arteriolar vasoconstriction. In HTN, the SNS has over activity which causes increased heart rate and systemic vasoconstriction which raises BP

81
Q

Coronary Artery Disease

A

atherosclerosis occludes the coronary arteries

82
Q

Myocardial Ischemia

A

when coronary blood flow is interrupted for an extended period, myocyte necrosis occurs

83
Q

Acute Coronary Syndrome

A

sudden coronary obstruction caused by thrombus formation over a ruptured or ulcerated atherosclerotic plaque

84
Q

ACS- Unstable Angina

A

Definition: result of reversible myocardial ischemia and is foretelling sign of impending infarction
Manifestations: ew onset angina, angina that occurs at rest, or angina that is increasing in severity or frequency. May have dyspnea, diaphoresis, and anxiety as it worsens

85
Q

ACS-STEMI

A

Definition: ST elevation that results in myocardial necrosis or injury. prolonged occlusion of coronary artery

Manifestations: sudden severe CP that radiates to neck, jaw, back, and shoulder, or left arm. “elephant sitting on my chest”

86
Q

ACS-NSTEMI

A

Definition: usually results from severe coronary artery narrowing, transient occlusion, or microembolization of thrombus and/or atheromatous material. less damage to heart then STEMI

Manifestations: SOB, pressure, dizzy, light headed, nausea, sweating, or pain or discomfort in your jaw, neck, back, or stomach

87
Q

Difference in clinical manifestation of older adults or those with diabetes who may have MI

A

No chest pain

Usually have unrelenting indigestion, nausea, and vomiting

88
Q

How might the structure and function of the heart change after a MI

A

After MI there is a functional impairment of the myocardium. Usually result in some degree of heart failure (pulmonary congestion, reduced myocardial contractility, and abnormal heart wall motion). Heart undergoes extensive myocardial remodeling leading to stiffness and distorts tissue structure leading to ventricular dysfunction.

89
Q

Reduced EF HF (left sided HF/systolic HF)

A

Etiology: inability of heart to generated an adequate cardiac output to perfuse vital organs

Risk Factors: coccaine, diabetes, high bp, obesity, tobacco, cardiomyopathy,

Clinical Manifestations: dyspnea, orthopnea, cough with frothy sputum, fatigue, decreased urine output, and edema. Inspiratory crackles, pleural effusions, S3 gallop, hypotension, hypertension

Pathophysiology: heart condition where the muscle on the left side of the heart is diminished and the pump doesn’t work to send blood body.

90
Q

Preserved EF HF (diastolic HF) right sided HF

A

Etiology: occurs alone or with systolic HF. Isolated preserved diastolic HF is defined as pulmonary congestion

Risk Factors: CAD, diabetes, obesity, pulmonary edema, pulmonary HTN, PE, pulmonic stenosis, alcohol, coccaine, high bp, sleep apnea, left sided HF

Clinical Manifestations: DOE, diastolic function is severe, pulmonary edema, inspiratory crackles, pleural effusion, S3 gallop

Pathophysiology: usually due to left side HF or pulmonary HTN. impaired contractility of the right ventricle caused by pressure, volume overload, or intrinsic myocardial contractile dysfunction

91
Q

Aortic Stenosis

A

Etiology: most common valvular abnormality caused by calcific degeneration d/t aging, congenital bicuspid valve, or inflammatory damage caused by rheumatic heart disease

Clinical Manifestations: angina, syncope, and heart failure, decreased stroke volume, reduced systolic bp, and narrowed pulse pressure. Heart rate often slow and pulses faint

Patho: lipoprotein deposits in the valve tissue with chronic inflammation and leaflet calcification

92
Q

Mitral Stenosis

A

Etiology: impairs the flow of blood from the left atrium to the left ventricle. Most common form of rheumatic heart disease

Clinical Manifestations: jugular venous distention , peripheral edema, atrial enlargement on xray, S1 sound can be accentuated and delayed, decreased cardiac output, heart murmur

Patho: inflammation leads to scarring of the valve leaflets; they become fibrous and fused which impede blood flow which results in incomplete emptying fo the left atrium.

93
Q

Aortic Regurgitation

A

Etiology: results from inability of the aortic valve leaflets to close properly during ventricular diastole, resulting from abnormalities of the leaflets or the aortic root or both.

Clinical Manifestations: widened pulse pressure, murmur, prominent carotid pulsations and bounding peripheral pulses

Patho: During systole some blood flow back into the left ventricle through a leaking valve. Volume overload occurs in the ventricle bec it receives blood from the atrium and the aorta during diastole.

94
Q

Mitral Regurgitation

A

Etiology: primarily due to mitral valve prolapse, rheumatic heart disease, infective endocarditis, MI, connective tissue disease, and dilated cardiomyopathy

Clinical Manifestations: caused by HF

Patho: permits back flow of blood from the left ventricle into the LA during ventricular systole, giving rise to loud murmur. As LA enlarges, the valve structures stretch and become deformed leading more backflow.

95
Q

Steps of myocardial ischemia

A

Myocardial ischemia occurs when blood flow to your heart is reduced, preventing the heart muscle from receiving enough oxygen. The reduced blood flow is usually the result of a partial or complete blockage of your heart’s arteries (coronary arteries). **partial blockage

–less than 20 minutes myocardial deficit&raquo_space; abnormal response to electrical impulses&raquo_space; dysrhythmias&raquo_space; sudden death OR impaired cardiac pumping with HF

96
Q

Steps of myocardial infarction

A

Blockage or build up of fat or cholesterol which forms plaque in the arteries. When the plaque ruptures and forms a clot that blocks blood, flow an infarct occurs

–greater than 20 min of myocardial deficit&raquo_space; lack of response to electrical impulses&raquo_space; failure to connect&raquo_space; impaired cardiac pumping&raquo_space; heart failure

OR

–greater than 20 min &raquo_space; abnormal response to electrical impulse&raquo_space; dysrhythmias&raquo_space; sudden death OR impaired cardiac pumping with HF

Adv Patho (23 decks)

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