Unstable angina: clinical features and diagnosis
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- Dyspnea, diaphoresis, and anxiety as the angina worsens
- EKG: will resolve with relief of pain
ST segment depression
T wave inversion
- Physical Exam:
, Transient 3rd and 4th heart sounds
Transient systolic murmur of mitral regurgitation
Non-ST-elevation MI (NSTEMI): pathophysiology
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- The infarction will involve only the myocardium directly beneath the
endocardium (subendocardial MI)
- Subendocardial MI causes ST depression and T-wave inversion (non-
STEMI)
Cellular changes r/t ventricular remodeling
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- Hypertrophy (abnormal myocyte growth)
- Intrinsic myocyte dysfunction
- Alterations in gene expression (proteins)
- Cell loss
- ECM remodeling
- Ca handling
- Mitochondrial dysfunction
Primary HTN: Increased cardiac output
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, Increased heart rate/stroke volume d/t any factors that increased
peripheral resistance/vascular tone, blood viscosity, or reduced vessel
diameter (vasoconstriction)
Increased preload and contractility can be caused by:
(1) Excess Na intake
(2) Renal sodium retention
(3) Fluid volume changes
(4) SNS overactivity
(5) Stress
Pathophysiologic mechanisms that mediate these effects:
(1) SNS
(2) RAAS
(3) natriuretic peptides
(4) Inflammation
(5) endothelial dysfunction
(6) obesity-related hormones
(7) insulin resistance
Fibrous-fatty plaque (evolves from fatty streak)
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- Accumulation of connective tissue
- Increased number of smooth muscle cells laden with lipids
- Deeper extracellular lipid pool
- Results in further endothelial cell dysfunction, necrosis of underlying
vessel tissue, and narrowing of the lumen as the lesion protrudes out from
the vessel wall
Hypertrophy
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Changes in the myocyte proteins, apoptosis of myocytes, and deposition
of collagen in heart muscle, that cause it to become thickened, scarred,
and less able to relax during diastole, leading to heart failure with
preserved ejection fraction.
Increased size of the heart muscle increases demand for oxygen delivery
over time, contractility of the heart is impaired, and the individual is at
increased risk for systolic heart failure
HDL risk levels for CAD (dyslipidemia criteria)
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<40 = low
≥60 = high
Other systems in HF
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Noncardiovascular entities such as renal failure, liver failure, morbid obesity
with peripheral edema, and chronic respiratory failure hypoventilation
syndrome may present with symptoms and signs that mimic HF
Factors in the Development of HTN: Metabolic syndrome
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- Dyspnea, diaphoresis, and anxiety as the angina worsens
- EKG: will resolve with relief of pain
ST segment depression
T wave inversion
- Physical Exam:
, Transient 3rd and 4th heart sounds
Transient systolic murmur of mitral regurgitation
Non-ST-elevation MI (NSTEMI): pathophysiology
Give this one a try later!
- The infarction will involve only the myocardium directly beneath the
endocardium (subendocardial MI)
- Subendocardial MI causes ST depression and T-wave inversion (non-
STEMI)
Cellular changes r/t ventricular remodeling
Give this one a try later!
- Hypertrophy (abnormal myocyte growth)
- Intrinsic myocyte dysfunction
- Alterations in gene expression (proteins)
- Cell loss
- ECM remodeling
- Ca handling
- Mitochondrial dysfunction
Primary HTN: Increased cardiac output
Give this one a try later!
, Increased heart rate/stroke volume d/t any factors that increased
peripheral resistance/vascular tone, blood viscosity, or reduced vessel
diameter (vasoconstriction)
Increased preload and contractility can be caused by:
(1) Excess Na intake
(2) Renal sodium retention
(3) Fluid volume changes
(4) SNS overactivity
(5) Stress
Pathophysiologic mechanisms that mediate these effects:
(1) SNS
(2) RAAS
(3) natriuretic peptides
(4) Inflammation
(5) endothelial dysfunction
(6) obesity-related hormones
(7) insulin resistance
Fibrous-fatty plaque (evolves from fatty streak)
Give this one a try later!
- Accumulation of connective tissue
- Increased number of smooth muscle cells laden with lipids
- Deeper extracellular lipid pool
- Results in further endothelial cell dysfunction, necrosis of underlying
vessel tissue, and narrowing of the lumen as the lesion protrudes out from
the vessel wall
Hypertrophy
, Give this one a try later!
Changes in the myocyte proteins, apoptosis of myocytes, and deposition
of collagen in heart muscle, that cause it to become thickened, scarred,
and less able to relax during diastole, leading to heart failure with
preserved ejection fraction.
Increased size of the heart muscle increases demand for oxygen delivery
over time, contractility of the heart is impaired, and the individual is at
increased risk for systolic heart failure
HDL risk levels for CAD (dyslipidemia criteria)
Give this one a try later!
<40 = low
≥60 = high
Other systems in HF
Give this one a try later!
Noncardiovascular entities such as renal failure, liver failure, morbid obesity
with peripheral edema, and chronic respiratory failure hypoventilation
syndrome may present with symptoms and signs that mimic HF
Factors in the Development of HTN: Metabolic syndrome
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