module 10 HTN and disorders Flashcards
preeclampsia
HTN during pregnancy
- 5-12% of pregnancies
- inc. risk of maternal, fetal, and neonatal morbidity and mortality
complications associated with preeclampsia
preterm labor abruptio placentae disseminated intravascular coagulation hemorrhagic stroke liver failure acute renal failure
aortic aneurysm
saclike enlargement in wall of aorta often assoc. with atherosclerosis
bulging -> inc. wall stress through inc. radius
-> dec. wall thickness -> red. ability to withstand stress.
Rupture: internal hemorrhage, fatal
Aortic aneurysm risk factors
HTN smoking obesity atherosclerosis hypercholesterolemia
dissection
aortic aneurysm
bleeding into the vascular wall through a tear in the inner layer (intima)
true aneurysm saccular
involves all 3 tunicae
ballooning on one side
true aneurysm fusiform
involves all 3 tunicae
ballooning on both sides
false aneurysm
at least one tunicae unaffected
- muscle tissue and fascia confine blood
- r/t trauma more often
hematoma
dissecting aortic aneurysm
tear creats channel for blood flow
- between intima and media or media and adventitia
- > inc. blood flow -> inc separation -> inc. weakness -> aortic rupture -> death
Atherosclerosis
endothelial dysfunction -> inflammation
oxidized LDL -> inflammation
foam cell formation (macrophage engulfs ox-LDL)
smooth muscle cell migration, proliferation, secretion
intimal thickening and atherosclerosis
smooth muscle cells migrate to intima
- cell mitosis
- elaboratoin of extracellular matrix (concrete that cell sits on)
clinical manifestations of systemic atherosclerosis (peripheral vascular disease)
skin - cool ot touch - dec. or absent hair - dry, thin, glossy appearance - thickened nails - pallor when elevated, rubor/blush when dependent - diminished pulses pain - sharp and stabbing - intensified with activity - relieved by rest or dependency Ulcer - severely painful - pale, gray base - well- defined edges - located on heels, lateral malleolus, distal phalanges, pretibial area
Atheroma/plaque
intimal lesion from fatty streak: lipid core covered by fibrous cap.
- Cells (smooth muscle cells, monocytes, and leukocytes), collagen, elastic fibers, and proteoglycans as well as lipids make up the fibrous cap.
- necrotic center: cell debris, cholesterol crystals, foam cells, calcium
atherosclerosis steps
damage to endothelium -> inflammatory response and inc. in vessel wall permeability
- > low density lipo-proteins breach intimal layer
- > lipids become oxidized -> further vessel damage
- > platelet aggregation -> release of growth factor
- > growth of smooth muscle cells in media layer
- > smooth muscle cells migrate to intima and proliferate
- > atherosclerotic plaque
- SMC, lipoproteins, and inflammatory debris
- > inc. plaque size -> dec. lumen size -> dec. perfusion
Atherosclerotic plaque rupture
- can lead to platelet aggregation and clot formation -> complete vessel occlusion (MI)
- Can also rupture without superimposed thrombus
atherosclerosis on supply and demand
coronary plaque - dec. perfusion - dec. arterial oxygen content increased demand - inc. HR - inc. preload - inc. afterload - inc contractility
risk factors for atherosclerosis
modifiable - smoking - HTN - glucose intolerance - elevated cholesterol and LDL - dec. physical activity - obesity - wt. fluctuations - ineffective stress management Non-modifiable - age - gender - ethnicity - heredity
3 layers of heart
epicardium: external
myocardium
endocardium: internal
ischemic heart disease
imbalance in myocardial O2 demand and supply supply < demand -> ischemia syndromes associated: - angina pectoris - acute MI - sudden cardiac death - chronic ischemic heart disease
angina pectoris
75% reduction in lumen.
intermittent chest pain d/t transient reversible myocardial ischemia
Stable: upon exertion
Variant: rest or in sleep
Unstable: increased frequency of pain
Platelet aggregation, vasoconstriction, and formation of mural (heart wall) thrombus -> dec. O2
Acute MI
Heart attack
complete occlusion
Sudden cardiac death
PE, ruptured aortic aneurysm, and infections
ventricular arrhythmias, in particular ventricular fibrillation
chronic ischemic heart disease
congestive heart failure
progressive form
degeneration of the myocardium with angina or myocardial infarction
s/s of acute MI
severe chest pain that may radiate may last several hours to days diaphoretic pulmonary edema cardiogenic shock
progression of necrosis during MI
caused by local ischemia
zone of perfusion, area that occlusion is depriving of O2
cells furthest away die off first.
lab evaluation during MI
creatine kinase: dimers M, B are found in derived from brain, myocardium, skeletal muscle tissue
- CK-MB primarily form the myocardium
- activity increases 2-4hr, peaks at 18, normal by 48
- Cardiac troponins T and I: more specific to heart cells
- increase after infarct but remain elevated 4-7 days
infarction
area of ischemic necrosis d/t occlusion of arterial supply or venous drainage
Classified based on color
- hemorrhage: red/white
- Microbial infection: septic/bland
preexisting collaterals
blood flow can get to a specific area multiple ways
- vessels connected
- blockage in one vessel, blood can “go around”
Management of blocked coronary arteries
- thrombolysis: drugs to remove thrombus
- percutaneous transluminal coronary angioplasty: scratches plaque off -> inflammation -> re-occulsion
- Placement of stent to prevent reocclusion
- coronary artery bypass, grafting a surgical placement of new conduit around occluded area
rate of coronary perfusion impaired by
large stable atherosclerotic plaque
acute platelet aggregation and thrombosis
vasospasm
failure of autoregulation by microcirculation
poor perfusion pressure
causes of Cardiomyopathy
"heart muscle disease" cardiac structural changes in disease - valvular disease -systemic or pulmonary HTN -heart failure - aortic stenosis - mitral incompetence
pulmonary hypertension and cardiomyopathy
right ventricular hypertrophy may occur in response to increased work of the right ventricle
aortic stenosis and cardiomyopathy
narrowing of aortic valve
- left ventricular hypertrophy occurs in response to greater work load
mitral incompetence and cardiomyopathy
left atrial dilation may develop as a result of the elevation of left atrial pressure and volume cause by mitral regurgitation
dilated cardiomyopathy
progressive form of cardiac hypertrophy associated with dilation and cardiac systolic dysfunction
- one or both ventricles
- Tends to affect all chambers of heart. 1 chamber -> all
dilated cardiomyopathy risk factors
alcohol toxicity
genetic component: dystrophin -> dec. contractility -> systolic dysfunction
pregnancy
postviral myocarditis
hypertrophic cardiomyopathy
asymmetric septal hypertrophy or idopathic hypertrophic subaortic stenosis
-abnml diastolic filling
- intermittent ventricular outflow obstruction
stiff thick wall -> impaired diastolic filling
hypertrophic cardiomyopathy risk factors
genetic: autosomal dominant
- abnormal sarcomere proteins
s/s of hypertrophic cardiomyopathy
septal hypertrophy
- strenous activity
- > inc. outflow obstruction
- > negligible SV
- > sudden death
- dyspnea
- angina
restrictive cardiomyopathy
rarest form
decrease in ventricular compliance -> impaired ventricular filling during diastole
-> dec. force of systole
dec. SV
common causes of restrictive cardiomyopathy
endomyocardial fibrosis cardiac amyloidosis (deposition of protein in wall) sarcoidosis glycogen storage disease iron overload scleroderma radiation inj
s/s of restrictive cardiomyopathy
exercise intolerance
dyspnea
weakness
congestive heart failure
build up of fluid
forward failure: systemic hypertension, mitral/aortic valve disease, ischemic heart
backward failure: venous backup
CHF pressure load
concentric hypertrophy
- heart working to overcome pressure
- > dec. chamber volume r/t inc. wall size
CHF volume load
eccentric hypertrophy
- increased volume in chamber
- dilation of chamber
compensated HF
maintain O2 in blood
decompensated HF
pulmonary congestion, edema, venous congestion, systemic edema
CHF s/s
dec. lung compliance during exertion
-> dyspnea
increased venous return -> orthopnea
cyanotic and/or acidotic
Left sided HF
most associated with LV infarction and systemic HTN backward effect - dec. ejection fraction -> inc. preload -> inc. atrial pressure -> pulmonary dysfunction -> inc. pressure in pulmonary veins and capillaries -> fluid forced into interstitial and alveoli -> edema forward effect: - dec. CO -> RAAS activation -> fluid retention -> dec. tissue perfusion
S/S of LSHF
cough crackles (rales) hypoxemia increased left atrial pressure blood tinged sputum and frothy cyanosis
acute cardiogenic pulmonary edema
life threatening associated with LHF
severely impaired gas exchange
s/s of LHF
severe dyspnea anxiety bolt-upright posture crackles throughout pink frothy sputum inc. HR tissue hypoxia
RSHF
LV failure -> inc. workload of RV -> RV failure isolated RV rare: r/t infarction or pulmonary disease - cor pulmonale: RV hypertrophy -> failure backward effect: - dec. ejection fraction -> inc. RV preload -> systemic congestion Forward effects: dec. output to left ventricle -> dec. CO -> dec. tissue perfusion -> RAAS activation -> fluid retention -> inc. RV preload
S/S of RSHF
Backward effects - hepatomegaly - ascites - splenomegaly - anorexia - subQ edema - jugular vein distention Forward Effects: - fatigue - oliguria - inc. HR - fait pulses - restlessness - confusion - anxiety
Cor Pulmonae
Heart disease caused by lung disease
result of pulmonary HTN
leads to cardiac hypertrophy and dilation
biventricluar HF
result of primary LV failure -> RSHF
dec. CO
inc. Pulmonary congestion
systemic venous congestion
