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CardioPul > path 1 > Flashcards

path 1 Flashcards

1
Q

describe the blood flow thru the heart

A
  • Right atrium
  • tricuspid valve
  • tright ventricle
  • pulmonic valve
  • pulmonic veins
  • left atrium
  • mitral valve
  • Left ventricle
  • aortic valve
  • aorta
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2
Q

Define Congestive Heart failure

A
  • characterized by variable degrees of DECREASED CARDIAC OUTPUT AND TISSUE PERFUSION, as well as pooling of bloodin venous system which may cause pulmmonay edema, peripheral edema or both
  • CHF occurs when the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do so only at an elevated filling pressure
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3
Q

What are the most common causes of Heart failure

A
  • Coronary artery disease –> myocardial infarction
  • High blood pressure
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4
Q

Define Acute Heart failure

A
  • Happens suddenly (think heart attack)
  • can be immediately life threatening because the heart doesn’t have time to undergo compensatory mechanisms
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5
Q

describe chronic heart failure

A
  • long term conditions
  • associated with the heart undergoing adaptive responses (DILATION, HYPERTROPHY) to a precipitating cause
  • these adaptive responses, however, can be deleterious in the long-term and lead to worsening condition
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6
Q

how is ultrasound used

A
  • looks at flow through the heart
  • allows for calculation of ejection fraction
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7
Q

Describe the Systolic dysfunction

A
  • Ejection fraction is LOW (heart is DILATED/ENLARGED VENTRICLES)

–> enlarged ventricles fill with blood

–> ventricles pump out less than 40-50% of blood (LOW EJECTION FRACTION IN SYSTOLE)

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8
Q

describe DIASTOLIC DYSFUNCTION

A
  • Ejection fraction is normal (thickened wall and LESS VOLUME)
  • The stiff ventricles fill with LESS BLOOD THAN NORMAL
  • The ventricels pump out about 60% of the blood (normal), but the amount may be LOWER THAN NORMAL (SYSTOLE)
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9
Q

What are the stages of CHF

A
  • Stage A = patietns at high risk for developing HF in the future but no functional or structural heart disorder
  • Stage B = a structural heart disorder but no symptoms at this stage
  • Stage C = previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment
  • Stage D = advanced disease requiring hospital-based support, a heart transplant or palliative care
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10
Q

describe the response to HF

A
  • Release of ATRIAL NATRIURETIC PEPTIDE (B-Type natriuretic peptide) –> over 100 = HF occuring
  • Activation of renin-angiotensin-aldosterone system (flow to kidney is reduced/low volume state)
  • Release of norepinephrine by adrenergic cardaic nerves of autonomic nervous system

–> increase HR and augment myocardial contractility and vascular resistance

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11
Q

describe Left sided CHF

A
  • Will produce SYMPTOMS

–> Dyspnea, orthopnea, paroxysmal nocturnal dyspnea

  • Pulmonary congestion and edema (HF cells present)
  • Dilation of left atrium
  • reduction in renal perfusion and CNS (in severe left sided CHF)
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12
Q

Describe Right sided CHF

A
  • Will produce SIGNS

–> Blood backs up into the venous system resulting in JVD, Pitting edema, congestive hepatosplenomegaly, pleural, pericardial or peritoneal effusions

  • usually results in pulmonary hypertension (cor pulmonale)
  • congestion of kidney and CNS
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13
Q

Describe Biventricular CHF

A
  • Both sides are failing, so combo of both
  • Most common cause of RIGHT HEART FAILURE is due to LEFT SIDED HEART FAILURE causing pulmonary edema leading to pressure on the rgiht heart leading to BIVENTRICULAR CHF
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14
Q

what are some treatments for CHF

A
  • Diuretics
  • angiotension converting enzyme inhibitors
  • Beta1-adrenergic blockers
  • mechanical assist
  • cardiac transplant (advanced, irreversible heart failure)
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15
Q

describe Ischemic heart disease (IHD)

A
  • MOST CAUSES CAUSED BY OBSTRUCTIVE ATHEROSCLEROTIC LESIONS in coronary arteries
  • Insufficient coronary perfusion relative to myocardial demand, due to chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries and variable degrees of superimposed acute plaque change, thrombosis and vasospams
  • SUBENDOCARDIUM IS MOST VULNERABLE
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16
Q

what are the modifiable and nonmodifiable risk factors for atherosclerosis

A
  • Nonmodifiable = incerasing age, male gender, family history, genetics
  • Modifiable
  • hyperlipidemia, hypertension, cigarrette smoking, diabetes
17
Q

describe the formation of Atherosclerosis

A
  • Endothelial injury/dysfunction causes binding of monocytes which will become macrophages

–> macrophages take up lipid and become foam cells which form fatty plaques

–> recruitment of smooth muscle cells precursors excrete extracellular martrix and fibroblasts

18
Q

describe vulnerable plaque

A
  • Soft with lipid filled core; most often eccentric; most often only 40-60% stenotic
  • Prone to rupture due to plaque hemorrhage or to fibrous cap disruption
19
Q

Ischemia vs Infarction

A
  • ISCHEMIA - reversible cellular injury

–> therapeutic salvage may be possible

  • Infarction - irreversible injury

–> myofiber coagulative necrosis

20
Q

what are the symptoms of IHD

A
  • Angina pectoris
  • myocardial infarction
  • chronic IHD with heart failure
  • sudden cardiac death
21
Q

describe Myocardial Ischemia

A
  • Define = insufficient oxygen supply to myocardial fibers
  • REVERSIBLE CONDITION, the result of:

–> decrease myocardial blood supply or..

–> increased myocardial oxygen demand

  • Diagnose via Tredmill test: see if they have angina during exercise
22
Q

Define stable (typical) angina

A
  • produced by physical activity, emotional excitement or any other cause of increased cardiac workload resulting in an imbalance in coronary perfusion relative to myocardial demand
  • relieved by resting or administering nitroglycerin
23
Q

Define Unstable or crescendo angina

A
  • pattern of increasing frequent pain, often of prolonged duration, that is precipitated by progressively lower levels of physical activity or that even occurs at rest
  • caused by disruption of an atherosclerotic plaque with superimposed partial thrombosis.
24
Q

define Prinzmetal variant angina

A
  • Episodic myocardial ischemia that is caused by coronary artery spasm
  • the angina attacks are urnelated to physical activity, heart rate or blood pressure
  • responds promptly to vasodilators, such as nitroglycerin and calcium channel blockers
25
Q

describe the ankle brachial presure index (ABPI)

A
  • ratio of the pressure difference from ankle to arm
  • ratio should be equal

–> when it starts reducing (lower pressure in ankle and higher pressure in arm) indicates peripheral vascular disease (atherosclerosis)

26
Q

describe teh symptoms of myocardial infarction

A
  • Chest pain - levines sign (clenchig their fist over sternum),

–> pain radiates to left arm, lower jaw, neck, right arm, back or epigastrium

Dyspnea

  • weakness, light-headedness, nausea, vomiting and palpitations
  • loss of consciousness and sudden death
27
Q

descrie the EKG changes in MI

A
  • ST elevation = MI
  • ST depression = Ischemia
28
Q

What happens with tissue death

A
  • Onset of myocardial infarction
  • plasma membrane of necrotic myocytes becomes leaky
  • molecules leak out of cell into circualtion

–> troponin will leak out and is measurable and indicates cell death (YOU DON”T GET IT WITH ISCHEMIA)

–> CK-MB is another marker to follow in order to make sure the patient does not REINFARCT

29
Q

Patient presents with chest pain OR anginal equivalent symtpom, how would you decide what it is.

A
30
Q

Why is timing so important in an MI

A
  • If you get to patient within 30 mins you can salvage the muscle and reperfuse the area (no muscle death)
  • If you want longer, the more cell death you develop
31
Q

What vessels are most likely to have an MI

A
  • LEFT ANTERIOR DESCENDING (40-50%)

–> infarcts involve the anterior wall of LEFT VENTRICLE near apex; anterior portion of ventricular septum and the apex circumferentially

  • RIGHT CORONARY ARTERY (30-40%)

–> infarcts involve the inferior/posterior wall of left ventricle; posterior portion of ventricular septuml and the inferior/posterior right ventricular free wall

  • LEFT CIRCUMFLEX (15-20%
  • Lateral wall of left ventricle except the apex
32
Q

describe histology post MI

A
  • 1-4 hrs = wavy fiber pattern
  • 12-24 hr = early coagulation and nerosis
  • 1-3 days = lots of neutrophils
  • 3-7 days = as neutrophils go away, the macrophages dominant

–> RISK OF MYOCARDIAL RUPTURE

–> switches from acute to chronic

  • OLDER = scar tissue develops
33
Q

What are the three scenarios leading to Myocardial rupture

A
  • Rupture of free wall of LV = CARDIAC TAMPONADE

–> decreases ability to fill and contract

  • Rupture of papillary muscle –> acute mitral valve incompetence

–> valvular disease suddenly

  • Rupture of ventricular septum –> acutely acquired VSD

–> ventricular septal defect (increases volume to lungs)

34
Q

Dressler’s syndrome

A
  • 2-weeks post myocardial infarction, but can be delayed for a few months

–> inner material leaks out and starts developing an immune reaction which leads to pericarditis weeks after MI

35
Q

describe pathogenesis of pericarditis

A
  • Can occur shortly after MI due to area of infarct rubbing against the peritoneum causing inflammation

CardioPul (11 decks)

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