Cardiovascular Disorders of the Human Body Flashcards
Endocardium
Inner most layer of the heart
Myocardium
Forms muscle layer between atria and ventricles, composed of myocytes
Pericardium
Outer layer: Tough, fibrous; resistant to distention by restricting left ventricle
Inner layer: serous; visceral (epicardium) & parietal layer
Pericardial cavity
contains 30-50 mL of serous fluid to lubricate/prevent friction
Autonomic Nervous System
SNS stimulation– Increases HR, controls smooth muscle tone of blood vessels
PNS stimulation– Decreases HR (vagus nerve), little/no control of blood vessels
SA Node
Pacemaker, 60-100 BPM, atrial systole
AV Node
40-60 BPM
Impulse travels down to eventually cause ventricular systole
Stroke Volume
The difference between end-diastolic & end-systolic volumes.
Ejection Fraction
Percentage of end-diastolic volume ejected w/ each heartbeat at systole. Normal = 60%. 30-40% is bad/HF
Cardiac Output
Is the amount of blood pumped by the ventricle per minute
CO=SV x HR
Ranges from 4 to 8 L/min
Frank Startling Law
Muscle stretching
Preload
The volume of blood in the ventricles at the end of diastole that the heart must pump w/ each beat
Determined by amt of venous return and degree of muscle stretch.
Afterload
The resistance or pressure the heart must overcome to eject blood from the left ventricle into the aorta. 184/100 BP.
Factors influencing CO
Cardiac Factors: HR, Contractility, Preload, Afterload
Renal, Fluid/Volume control
Renin-Angiotensin
Aldosterone
Atrial Natiuretic factor: released when there’s too much volume
Primary Hypertension
Essential or idiopathic hypertension/Silent Killer
Occurs without evidence of other disease
Affects 90% to 95% of individuals with hypertension
Blood pressure of 140/90 mmHg or higher
Some of the common causes:
Overactive SNS (sympathetic)
Secretion of norepi release of adrenaline (Epi) from adrenal medulla increase BP
Overactive Renin-angiotensin-aldosterone system
Salt and water retention & increased vascular tone
Insulin resistance/Metabolic Syndrome
Secondary Hypertension
Kidney disease- most common cause is renal artery stenosis
Hyperthyroidism
Hypersecretion of aldosterone or catecholamines
Pheochromocytoma: cancer of adrenal gland
Pregnancy induced hypertension (PIH)
Clinical Manifestations of Hypertension
S/S often secondary to TOD:
HeadAche, blurred vision, fatigue, dependent edema, palpitation, angina, dyspnea
Complications: Specific target organ damage Cerebral vascular disease (stroke) Cardiac disease (CAD, LVH, Heart Failure) Peripheral Arterial Disease (PAD) Renal damage Retinal damage
Orthostatic (postural) Hypotension
Decrease in both systolic and diastolic blood pressure upon standing
Drop in SBP≥ 20mmHg / DBP ≥ 10mmHg
Lack of normal blood pressure compensation
Reduction of blood flow to brain
Vasodilation, pooling of blood in blood vessels of the lower extremities
S/S: Dizziness, blurred vision, syncope
Hyperlipidemia
RISK FACTORS
Genetic predisposition (primary or “familial” )
Age (over age 45 in men and age 55 in women)
Diabetes & hypothyroidism (↑ triglycerides)
Gender (after menopause, women’s LDL levels tend to rise)
Certain medications
High dietary intake of cholesterol (↓LDL receptor formation & activity = ↓ LDL removal)
Obesity
Cholesterol
Cholesterol and triglycerides are the two main lipids in blood. The body uses cholesterol, an essential component of all cell membranes, to form steroid hormones and bile acids. The liver produces most of the body’s cholesterol, but an estimated 20-40% comes from food sources.
Must be carried by lipoproteins (LDL)
High Density L picks up cholesterol and takes it to liver
Clinical Manifestations of Hyperlipidemia
Atherosclerosis Coronary artery disease Stroke Peripheral artery disease High Blood pressure
Diagnosing Cholesterol/Hyperlipidemia
LDL: Less than 100
HDL: Between 40-60
Total: Less than 200
Treatment of Hyperlipidemia
Reduce caloric intake, saturated & trans fats, & cholesterol
Increase intake of soluble fiber
Daily exercise (at least 30 minutes a day)
Weight reduction if overweight or obese
Smoking cessation
Lipid-lowering medications
Atherosclerosis
Significant correlation to Hyperlipidemia
Thickening and hardening is caused by accumulation of lipid-laden macrophages in the intimal wall of the artery
Most common in: Aorta, coronary arteries, and large vessels of the brain
Plaque development (LDL cholesterol, lipids, inflammatory response)
Formation of fibrofatty lesions in the intimal lining of the large and medium-sized arteries, and the large vessels that supply the brain
Atherosclerosis (in a nutshell)
Lipids get into the vascular endothelium
White blood cells try to clear them away foam cells
WBCs (monocytes→activated macrophage) release growth factors that promote plaque formation in the vascular endothelium
Risk Factors for Atherosclerosis
Modifiable: Hypercholesterolemia (Hyperlipidemia), Hypertension, Cigarette smoking, Sedentary lifestyle
Type II diabetes
Non-modifiable: age, genetics, CHD, males (45 yrs), females (55 yrs), High homocysteine levels
Clinical Manifestations for Atherosclerosis
Ischemia caused by vessel narrowing Thrombus and formation of emboli Infarction caused by vessel occlusion (coronary & cerebral arteries) Aneurysms and dissections Peripheral artery disease (PAD)
Atherosclerosis Treatment
Reduction of risk factors: high cholesterol, high blood pressure, Type II diabetes, dietary modifications
smoking cessation
Peripheral artery disease and Intermittent Claudication
Peripheral artery disease
Atherosclerotic disease of the arteries that perfuse the limbs
Intermittent Claudication:
Primary symptom of chronic obstructive arterial disease
Ischemia (lack of O2) to the calf, especially during walking or exercise
Pain is relieved with rest
If pain occurs at rest, condition is worsening and may lead to ulceration and gangrene
Weak/absent pulses in lower extremities
Hair loss
Raynaud disease
Vasospastic disorder of unknown origin
Possible hyperreactivity of SNS
Raynaud phenomenon
Can be secondary to other systemic diseases or conditions or associated w/ previous vessel injury
Collagen vascular disease (scleroderma), smoking, pulmonary hypertension, and environmental factors (cold and prolonged exposure to vibrating machinery)
Thromboangiitis Obliterans (Buerger disease)
Vasculitis of medium-sized arteries Arterial ischemia, especially to distal extremities (mostly the foot or lower leg) Most common in men (before age 50) Most common to individuals who smoke Painful, cyanosis to extremities
Aneurysm
Local dilation or out-pouching of a vessel wall or cardiac chamber
Most common to arteries
Most common to Aorta
Most commonly caused by atherosclerosis & HTN
Aortic dissection (medical emergency)
Tear in intimal layer of aorta, disrupting flow through arterial branches
Associated with:
Chronic HTN
Trauma to the aorta
S&S
Sudden excruciating pain (“tearing” of “ripping”). Chest &/or back
Syncope, hemiplegia, paralysis of Lower Extr
Pericardial Effusion
Result of injury & inflammation
Sudden accumulation of fluid and increase in intrathoracic pressure impede venous return to the heart and constricts !
Cardiac tamponade: Life-threatening!
Decreased ventricular diastolic filling …decreased SV…decreased CO…decreased SBP…circulatory shock
Pulsus paradoxus- KEY diagnostic finding
Acute Pericarditis
Increased capillary permeability…leakage of plasma proteins into pericardial space
Chest pain, sitting up relieves pain
Constrictive Pericarditis
Scar tissue between visceral & parietal layers interfere w/ diastolic filling
