alterations cv function

50

80

Pooled blood in veins, caused by trauma or gradual venous distention

prone to ulceration with pooled blood in extremities.

Triad of virchow:
Venous stasis (imobility age, chf)
Vein endothelial damage (trauma, meds)
Hypercoagulable states (HRT, oral contracept, maignancy)

r V linden mutations; Prothrombin mutations; Deficiency of protein C and S and anti-thrombin

- early ambulation
- SCD type devices
- prophylactic meds (heparin, etc)

– venous distention of upper extremiies and head.
Oncologic emergency – not venous emergency

aka: essential or idiopathic
95% cases

Stroke volume: amount of blood ejected by every beat
Preload
Afterload
Contractility

Consistent increase of systemic arterial blood pressure.

systolic bp (top number)

= hypetention, dyslipidemia, glucose intoelrance and obesity

Nicotine is a vasoconstrictor and inc SBP/DBP acutely

Risk of HTN higher if ETOH intake >> 3 drinks/day, however 1-2 drinks decrease daily SBP/DBP

protein. genetic mutation/deficiency increases the risk of HTN by 50%-70% in white population due to messing wtih Na/K pump and ATP

Sustained increase in peripheral resistance ( arteriolar vasoconstriction), Increased circulatory blood volume or both

Increase in HR and vasoconstriction, structural changes in blood vessels, Na and H20 retention, Increase in renin , ANG plus pro-coagulant effect

Arteriolar remodeling, increase in peripheral resistance, end-organ effect: atherosclerosis, renal damage and cardiac hypertrophy

Insulin resistance: Inc in endothelial release of NO ; renal retention of Na/H20 , activate SNS and RAA.

Elevations of systolic pressure are caused by increases in cardiac output, total peripheral vascular resistance, or both

Pulse pressure (PP)= SBP- DBP.
Increase in PP= decrease in vascular compliance so PP always increased in isolated systolic bp

- ventricular hypertrophy
- angina
-MI
-sudden death

chronic hypertension wtih multiple target organ damage

DBP greater than 140
- May lead to papilledema, cardiac failure, uremia, retinopathy and CVA

high SBP (>180) but needs to be lowered slowlly to avoid stroke

dislodgement of
- thrombus
- air bubble
- aggregate fat
- bacteria
- cancer cells

vasospastic disease in arterioles/arteries

Collagen vascular disease (scleroderma), smoking, pulmonary hypertension, myxedema, and environmental factors (cold and prolonged exposure to vibrating machinery)

Chronic disease of arterial system
Blood vessel thickening accumulation of lipids
Involve lipids, choolesterol
Related to HTN, perfusion insufficiency
Form of atherosclerosis (most common)

Atherosclerosis progression
Inflammation of endothelium (smking, HTN, DM, etc)
Cell proliferation
Micarophage migration
LDL oxidation (foam cell formation)
Fatty streak
Fibrous plaque
Complicated plaque

key step in formation of atherosclerosis

Any condition causing occlusion of the coronary arteries
Atherosclerosis most common cause

Key step in atherosclerosis: Oxidized LDL enters the vessel wall, phagocytosis by macrophages

reverse cholesterol transport”. Takes excess cholesterol in the periphery back to the liver for metabolism

MOA is not certain, however it is a vasonstrictor, increases in HR , catecholamine's and increases Peripheral vascular resistance ( PVR)

multiple mechanism- endothelial damage, increased inflammation and thrombosis; associated with dyslipidemia

Coronary arteries occluded by more than half - starts 10 seconds after occlusion

transient ( 3-5 min). Pain due to lactic acid build up. Mostly due to gradual narrowing of lumen and hardening arterial wall

transient, unpredictable and often at rest. Due to vasospasm of coronary arteries with/without atherosclerosis

asymptomatic. Common in women. Global or regional abnormalities in LV sympathetic innervation

Increased BP, myocardial oxygen demand
Chronic stress will lead to hypercoagulable state and thrombosis
“silent angina”
Stress management in men has resulted in great reduction in CV events

Reversible ischemia: Fissure or superficial erosion of plaque causes transient vessel occlusion and vasoconstriction at site of plaque damage. Occlusion lasts 10-20 min with return of perfusion before myocardial necrosis
- ekg ST segment depression and T wave inversion
- 20% patients have MI/sudden death

- Thrombus breaks up before complete distal necrosis. Only involves myocardium beneath endocardium ( i.e. subendocardial ) is impacted.
- minor MI

Thrombus lodges permanently and necrosis extends through myocardium ( from endocardium through epicardium) resulting in sever cardiac dysfunction

Structural and functional changes- Ejection fraction drops and there will be increase in ventricular end diastolic volume: If obstruction involves perfusion to LV then there will be Pulmonary venous congestion. If RV is ischemic then there will be increase in systemic venous pressure

temp loss of contractility

persistent ischemia , metabolic adaptation to help myocardial survival

catecholamine's, ANG II, Aldosterone, other inflammatory mediator- myocyte hypertrophy

- Cellular injury- myocardial cells withstand ischemia for 20 min.
- After 30-60 sec of hypoxia there will be EKG changes
- Within 8 sec myocardial oxygen reserve is used
- Glygogen stores fall and anaerobic metabolism starts but falls short..i.e. only 65% to 70% of myocardial demand for ATP is met.
- Hydrogen ions and lactic acid build up lead to acidosis leading to conduction and contractility impairment
- Myocardial cells release catecholamine's, increase in ANS activity and abnormal heart beat. Fatty acid and glycerol increase within 1 hour. - Norepinephrine release increases Blood sugar
- ANG II causes LV remodeling and also causes coronary artery spasm, vasoconstriction, fluid retention

General term used to describe several types of cardiac dysfunction that result in inadequate perfusion of tissues with blood-borne nutrients

heart failure - most common cause

Volume of blood ejected per beat and is dependent on 3 factors:
Pre-load
Afterload
Contractility

amount of blood ejected by ventricle = 60% to 75% for Normal resting heart
EF = SV/ Ventricular end diastolic volume (VEDV)

Volume and associated pressure generated at the end of ventricular diastole (VEDV and VEDP) and is determined by two factors:
- Venous return
- End systolic volume

Ventricular wall tension to produce intraventricular pressure depends on the size of ventricle. i.e. VEDV determines the size and stretch (force) of contraction
- more stretched -less systemic pressure

Load muscle must move after it starts to contract.
Resistance or impedance to ejection of blood from the ventricle.
In HF, it takes higher filling pressure to accomplish normal contractile force

- will lead to decrease in Stroke volume and increase in VEDP.

causes “back up” into pulmonary ( pulmonary edema) or systemic venous circulation ( peripheral edema

dec Contractility. ..dec Stroke volume…Inc VEDV ( dilation of heart)…Inc preload which in long-term stretches the myocardium and cause loss of contractility