Exam 2 Flashcards
L sided HF
- Decreased contractility of LV
- decreased SV, EF, and CO
- increased EDV and LV EDP
- can lead to pulmonary congestion/edema
R sided HF
- Decreased contractility of RV
- accumulation of blood in RV, RA, and systematic circulation
CHF
- Combo of R and L sided HF - overall decreased ventricular contractility
- due to changes in myocardium, heart can’t meet metabolic demands
HF staging
A: pre-HF
B: has disorder; no symptoms
C: has disorder and symptoms; medical management
D: has disorder and symptoms more advanced
Acute HF
- 5 lb rule; gain 5 lbs in 24 hrs is an acute episode
- rapid onset of symptoms
systolic HF or HFrEF
- REDUCED EF and oxygen delivery to tissues
- decreased LV contractility
diastolic HF or HFpEF
- preserved EF
- ventricles lose their ability to relax and become stiffer and less compliant
- chambers don’t fill normally during diastole
- reduced volume capacity of chambers
ischemia
restricted/reduced blood flow
hypoxia
a condition in which a body/region is deprived of adequate O2 supply at the tissue level
hypoxemia
low O2 content in blood
Acute Coronary Syndrome
- non specific dx
- sudden decreased blood flow to heart
Ischemic Heart disease
- under ACS
- includes MIs, stable/unstable angina, atherosclerotic injury to coronary arteries
IHD diagnosis
cardiac enzymes, C-reactive proteins, homocysteine, abnormal lipid profile, brain natriurtic peptide, prothrombin
ischemic cardiomyopathy
- ischemia to to heart muscles
- causes decrease in contractility
- if chronic, damage to myocytes is irreversible and cardiac remodeling occurs
- ultimately may develop CHF
Cardiac and RA
- presence of RA is considered primary pathogenic factor for premature development of atherosclerosis
- increased risk x3 of CV event
IHD- angina
-intermittent chest pain caused by transient, reversible myocardial ischemia
stable angina
- O2 delivery is not meeting O2 needs
- onset: increased exertion of stress
- occurs at PREDICTABLE HR
- Tx with nitrates or decreased stress
unstable angina
- onset: exertion or stress
- onset is UNPREDICTABLE
- Tx with nitrates potentially
- can occur due to plaque changes and/or coronary artery vasospasm
IHD- MI
Time is Tissue
-ischemic insult for long period of time leading to tissue damage and tissue/whole body death results
IHD- sudden cardiac death
- cessation of cardiac function
- Pathology ventricular fibrillation –> Asystole
- Potential causes: quiet MI, acute coronary plaque rupture/thrombus, >60% narrowing of artery
IHD pathogenesis
- originates from plaque in arterial lumen due to inflammation and lipid deposits
- plaque rupture- exposes plaque to blood
- occlusive event- damage dependent on coronary artery involved, time until treated
Poiseville’s Law
- blood flow regulation
- Q=chang in Pxr^4
- if radius decreased, resistance increases, pressure increases
- results in decreased blood flow
Double product
- blood flow regulation
- DP= HR x systolic BP
- tells us how hard the heart is working
- could indicate co-existing CV conditions with risk of AE
Primary HTN
90% of all cases
no known cause
-progressive, decreased vascular compliance
Secondary HTN
caused by kidney conditions, arterial, heart, or endocrine conditions
10% of all HTN cases
HTN and Kidney disease
- decreased blood delivery to kidney tissue
- arteries around kidney narrow, weaken, and harden
- decreased filtration; increased water retention
- increased BP
- increased pre-load
- increased total peripheral resistance
- decreased ability to control BP
HTN and diabetes
- elevated glucose levels damage glomerular filtration
- increased water retention and increased volume and BP
HTN and heart disease
- increased afterload - lead to thickened heart and thickened BV walls
- causes changes in the heart making it less effective
- LV progressively dilates and thins walls; leading to declining EF
Cor Pulmonale
- enlargement of R ventricle caused by pulmonary HTN
- chronic and progressive
pulmonary HTN
- causes cor pulmonale
- MAP >25 mmhg or systolic pressure >35mmHg
lung diseases and CP
- COPD
- diffuses pulmonary interstitial fibrosis
- collapsed lung
- cystic fibrosis
- PE
Pulmonary vessels and CP
- pulmonary vascular sclerosis
- drug, toxin, radiation induced vascular sclerosis
CP Clinical Implications
PT- low impact, light-mod resistance
-try not to overexercise
Assessment Criteria for taking BP
- rest 5 min
- legs uncrossed
- feet on floor
- arm supported
- cuff size
- cuff on bare arm
- no talking
- no phone/ reading
- take BP on both arms
- record higher BP reading
- record which arm to use for future readings
cardiomyopathy
- disorder WITHIN the cardiac myocytes affecting performance
- irreversible decline of cardiac function
- long term pts often look for transplant
- resulting in reduced EF
dilated CM
- most common form of myopathies
- chamber dilation/enlargement along with contractile impairment
- decreased EF and SV
- dilated heart undergoes remodeling
- LV “ballooning” causing dilation of other chambers
- ultimately leads to HF
dilated CM remodeling
-heavier than normal heart
-hypertrophies myocytes
-loss of myofibrils, reduced mitochondrial function
-fibrosis
thin-walled chambers
causes of dilated CM
- genetic mutations
- viral infections - HIV
- toxins- ETOH, cancer drugs, cocaine
- metabolic disorder- DM, nutritional deficiencies, hyper/hypo thyroidism
- myocarditis
hypertrophic CM
- most common cause of death
- thickened LV with a non-dilated LV chamber
- functionally defective myocytes- abnormally high BPs is THEIR normal BPs
- LV and septal walls hypertrophy to compensate
- ultimately heart will decompensated- decrease functional capacity and fail
obstructive HCM
septal wall thickens and LV wall stiffens, obstructing blood flow into the aorta
nonobstructive HCM
LV wall stiffens and reduces LV EDV and SV
-blood flow is not blocked
HCM long term complications
- atrial fibrillation
- dysrhythmias
- HF
- Hx of MIs
Restrictive/infiltrative CM
- restrictive diastolic filling/ loss of compliance; chambers unable to expand
- systolic function is normal
- EDV and SV is reduced
- ESVs and EFs normal
- increased pressure in ventricular filling
Restrictive CM causes
- scleroderma
- amyloidosis
- sarcoidosis
- Diabetes
- hemochromatosis
- Chemo agents
- radiation exposure
Pneumonia
-an acute lung injury where inflammatory process affects parenchyma of the lungs
Pneumonia causes
- bacterial, viral, and fungal infections
- inhalations of toxins, chemicals, smoke, dists, gases
- aspiration of food, fluids and vomit
Pneumonia pathogenesis
- inflammatory and immune responses with damaging SEs to lung tissue
- endotoxins released that damage bronchial and alveolocapillary membranes
- damage type II cells
tuberculosis
- mycobacterium tuberculosis
- site of infection: lungs, vertebral column (Pott’s), CNS, heart
- transmission: airborne; casual contact insufficient; household exposure over many months more likely
tuberculosis progression
- infection in lungs
- epithelial cells surround and encapsulate replicated bacteria to limit further spread (granuloma)
- TB in Ghon complex can be reactivated- secondary infection
- cavity is formed in tissue where immune cells cant reach
- pt becomes infectious
Obstructive lung disease
- conditions that makes it hard to EXHALE all the air in the lungs
- caused by aspiration, PE, Emphysema/chronic bronchitis
- Identified via pulmonary function tests
COPD
- Chronic obstructive pulmonary disease; a non-specific dx
- includes emphysema, chronic asthma, and chronic bronchitis/small airways disease
- 3rd leading cause of death
COPD and spirometry
- test pulmonary function and lung volumes
- diagnostic and prognostic
- Dx: FEV1/FVC ratio is <0.70 following bronchodilator administration
FEV1
amount of air you can force OUT of your lungs in 1 sec
FVC
total amount of air exhaled out of your lungs after taking a deep breath
Obstructive Lung disease: emphysema
-pathologic accumulation of air in lungs; air is trapped in lungs
-Increase in residual volume, total lung capacity
decrease in FVC1/FVC ratio
-TLC- flattened diaphragm compromising function
Emphysema causes
- Genetic- Alpha-1 atitrypsin deficiency
- cigarette smoke- can affect alpha-1 atitrypsin function
Effects of A-1 AT deficiency and cigarette smoking
- destruction of individual alveoli
- development of “super alveoli”- causes air trapping
- destruction of connective tissue supports for the very smallest airways allowing them to collapse during expiration
Emphysema FEV1/FEV
Pink puffer
- accompanied heart problems or cor pulmonale
- ineffective cough
- hypoxemia
- hypercapnia- retaining CO2
- chronic pumonary metabolic acidosis
- deconditioning
chronic bronchitis
- productive cough lasting at least 3 months per year for 2 consecutive years
- increased mucous production causing obstructed airflow
- inflammation and scarring
chronic bronchitis FEV1/FEV dx
<75% WITH chronic cough
Blue bloaters
- chronic bronchitis
- decreased ventilation
- increased RV and decreased expiratory flow
- shunting
- hypoxemia, hypercapnia, cyanosis, polycythemia
- cor pulmonale
Asthma
- episodic, reversible, obstructive lung disease due to bronchospasms
- exaggerated inflammatory response to smooth muscles to stimuli
extrinsic asthma
- allergic
- mast cells degranulate and release histamines causing inflammatory response and smooth muscle constriction
intrinsic asthma
- non-allergen/ non-immune response
- adult onset
- often secondary to chronic or recurrent infections of the bronchi, sinuses, tonsils or adenoids
Asthma pathogenesis
- an inflammatory response
- inflammatory mediators
Bronchial Provocation test
- administration of methacholine to cause smooth muscle contraction
- evaluates airway sensitivity
- (+) test 20% decrease in FEV1
