Patho Cardiovascular

100問 • 2年前

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Transport blood under high pressure from the heart to the capillary bed of tissues (high pressure/thick muscular walls)

Arteries

Small branches of arteries that act as conduits between arteries and the capillary beds of tissues (muscular walls and sphincters)

Arterioles

Extensive lattice of vessels that supply blood to the cells/areas of substrate exchange (thin walled with pores for permeability)

Capillaries

Collect blood from the capillaries and coalesce to form veins

Venules

Transport blood from the Venules back to the heart. Act as a reservior (low pressure system, thin walls)

Veins

Anount of blood in venous system

64%

LCA branches into?

Left anterior descending artery and Circumflex artery

Left Anterior Descending Artery provides blood to?

LV and RV, Intraventricular septum

Circumflex Artery supplies blood to?

LA and Left lateral wall of LV

Right Coronary Artery supplies blood to?

RV, Intraventricular sulcus, and small vessels of RV and LV

Relaxation and Filling of the Heart

Diastole

Contraction of the Heart

Systole

Flow (Q) through a blood vessel determined by?

Pressure difference between two ends of a vessel, Resistance (diameter), Viscosity, and Length of vessel

Flow of blood to lungs: Flow of blood to body

QP:QS

Measurement of Vascular Resistance

Woods Units

<8 weeks of age = 8-10 woods/m2. >8 weeks of age = 1-3 woods/m2.

Pulmonary Vascular Resistance (PVR)

Infant = 10-15 woods/m2. 1-2 yrs old = 15-20 woods/m2. Child-Adult = 15-30 woods/m2.

SVR

How easy it is for blood to travel through arteries

Compliance

Constriction and Relaxation of Smooth Muscle of Arteries and Arterioles controlled by:

Sympathetic Nervous System, Local Tissue Metabolism, Hormone Response, Changes in Chemical Environment

Comparing Catecholamines

Epinephrine has more Alpha1, Beta2, and Beta3 receptor action than Norepinephrine

Comparing Catecholamines

Norepinephrine has less receptor action on cardiac output and heart rate than Epinephrine but the same effect on coronary blood flow

Comparing Catecholamines

Epinephrine and Norepinephrine have the same effect on Systolic BP but Norepinephrine has more effect on Diastolic BP

Volume of blood returning to the heart from systemic circulation = RA pressure or CVP

Preload

Systemtic pressure = pressure the heart must pump against to circulate blood = MAP

Afterload

Contraction units of Cardiac Muscle

Myofibrils

Thin protein filament, light band or I band (isotopic)

Actin

Thick protein filament, dark bands or A Bands (anisotropic), small projections from sides that form cross-bridges

Myosin

Site of connecting myofibrils

Z-Discs

Portion of myofibrils between two Z-Discs

Sarcomere

Helix backbone, F-actin and G-actin

Actin

The active site for cross-bridges with myosin

G-actin

Protein wrapped around F-actin, blocks active site

Tropomyosin

Three subunits of Troponin

Troponin I, T, and C

Affinity for actin

Troponin I

Affinity for Tropomyosin

Troponin T

Affinity for Calcium

Troponin C

Two polypeptide chains wrapped in spiral forming a double helix

Myosin Tail

Globular polypeptide with associated light chains

Myosin Head

Individual Myosin Molecules Bundled Together to Form the Body Where Cross-Bridge Hangs

Myosin Filaments

Flexible Hinge and Arm Connected to Myosin Heads

Myosin Cross-Bridge

Enzyme in Head for Energy Production

ATPase

Myofilament and Actin Interaction

At rest, active sites on actin are blocked troponin and Tropomyosin complexes. During action potential, troponin C binds with calcium and moves the complexes off of the actin active site. Actin and myosin interact causing muscle contraction.

Walk-Along Theory

Head myosin cross-bridge attached to the actin filaments at the active site. Intra-molecular forces cause the myosin head to tilt forward on a flexible hinge and drag the actin filament with it (power stroke). Myosin head breaks away and interacts with the next actin site. Z-disc pulls filament together at the sarcomere —> muscle contraction. ATP is cleaved to fuel process.

Potassium concentrations in cell

High inside cell membrane, low outside cell membrane

Diffusion of Potassium

Diffuses out of the cell causing negative intracellular charge

Concentration of Sodium in the Cell

Low inside the cell membrane, High outside the cell membrane

Diffusion of Sodium in the Cell

Sodium diffuses into the cell causing a positive intracellular charge

At rest cell has?

Negative charge

Leak of sodium into the cell, decreases the intracellular negativity. Opens voltage gated ion channel to generate more positive ion (Na and Ca) entry. Cell becomes more positive. Action potential is generated.

Depolarization

Potassium rapidly diffuses out of the cell and the intracellular negativity increases to resting state.

Repolarization

Phases of Action Potential

0: Depolarization; 1: Early Repolarization; 2: Plateau (Repolarization)-Na and Ca slowly enter cell; 3. Potassium moves out of cell; 4: Return to resting potential.

Time cardiac muscle is refractory to additional stimulation

Refractory Period

Site of automaticity due to slow leak of NA ions (the most Na leak channels) that slowly increase intracellular charge until action potential is fired releasing Ca from the muscle fibers to cause myosin/actin contraction

SA Node

Spread of depolarization through atria, followed by atrial contraction

P wave

Pause in Conduction at AV Node

PR Interval

Deopolarization of the ventricle, followed by ventricular contraction

QRS complex

Repolarization of the ventricles, happens just before the end of ventricular contraction

T wave

Amount of blood in a heart chamber after filling, before systole

End-diastolic volume

Amount of blood ejected with each contraction of the heart

Stoke volume

Amount of blood that remains in the heart chamber after systole

End-systolic volume

Percent of blood in chamber that is ejected with each systole

Ejection fraction

Amount of blood pumped into the aorta each minute

Cardiac output

HR x Stroke Volume

Cardiac output

P rate > 300, no PR interval, QRS variable, irregular rhythm. Decreased filling time causing fatigue? dizziness, dyspnea, irregular pulse

A-Fib

Associated with things that remodel the atria: (HF, ischemic CV disease, HTN, Obesity, OSA, rheumatic heart disease)

A-Fib

Early beats without p waves. Effects: decreased CO from loss of atrial contribution to ventricular preload resulting in heart fluttering, pounding, and palpitations. Associatied with abnormal potassium, hypercalcemia, hypoxia, aging, anesthesia, caffeine, tobacco, illicit drugs, exercise

PVCs

Role of Lipoproteins

Manufacturing and repair of plasma membranes and cholesterol for bile salts and steroid hormones

Dietary fat packaged in small intestine—> chylomicrons —> liver —> processed into:

Very-low-density lipoproteins (triglycerides), Low-density lipoproteins (LDL), High-density lipoproteins (HDL)

Strong predictor of cardiac events

Very-low-density lipoproteins (triglycerides)

Indicator of cardiac risk but in context of other factors (age, diabetes, CKD)

Low-density lipoproteins (LDL)

Protective against atherosclerosis- want high level to remove access cholesterol from arterial walls

HDL

Primary causes of dyslipidemia

Genetics from abnormal lipid metabolism and cellular receptors

Secondary causes of Dyslipidemia

Lifestyle, HTN, DMII, Hypothyroidism, Pancreatitis, Renal Nephrosis, Chronic Inflammation, Diuretics, beta-blockers, steroids, antiretrovirals, air pollution, radiation, microbiome

Chronic inflammation resulting in damage to arterial walls and plaque formation

Atherosclerosis

Lesion in arteries filled with lipids and marcophages (stable or unstable)

Plaque (atheroma)

Step 1 of Atherosclerosis

Injury to endothelium—>inflammatory response—>monocytes and platelets move to site of injury

Step 2 of Atherosclerosis

LDL enters the intimas layer of the vessel—>inflammation + oxidative stress + macrophage activation—> engulf LDL = foam cells —> foam cell accumulation = fatty streak

Step 3 of Atherosclerosis

Further inflammation process in response to fatty streak—> smooth muscle cells produce collagen —> form over fatty streak making a plaque (May calcify = Monckeberg atherosclerosis)

Unstable plaques prone to rupture

Complicated lesions

Atherosclerotic disease of the arteries

Peripheral artery disease

Pain without ambulation found in PAD

Intermittent claudication

Contributes to blood pressure regulation, promotes cardiac contactility, controls arteriolar vasoconstriction (peripheral vascular resistance)

Sympathetic Nervous System

Responds to Catecholamines (epinephrine and norepinephrine), stimulates renin-angiotensin system (RASS)

Sympathetic Nervous System

Hypertension

Sustained BP 130/80

95% of HTN caused my genetics and environment

Primary HTN

Caused by underlying disease process (renal, pheochromocytoma, pregnancy) increasing PVR and CO

Secodary HTN

Vascular remodeling—> fibrosis of vessels—> organ injury (cardiac muscle, retina, kidneys, brain). LV Hypertrophy-> HF.

Complications of HTN

Rapid increase in SBP> 140mmHg—> cerebral arterioles cannot regulate blood flow to cerebral capillaries—> cerebral edema—> encephalopathy

HTN Crisis

Associated with pregnancy, cocaine and meth use, adrenal tumors, ETOH withdrawal

HTN Crisis

Supports Sodium Excretion

K, Mag, Ca

Deposited in tunica media and assists with vasoconstriction and increasing BP

Direct vasodilator lowering BP

Mag

Atherosclerosis of coronary arteries. Diminished blood supply.

CAD

Local, temporary oxygen depravation. Cells live but cannot function normally.

Persistent ischemia or complete occlusion of coronary artery. Commonly myocardial infarction.

Acute Coronary Syndromes

Dyslipidemia, HTN, Smoking, DMII, Insulin Resistance, Obesity, Diet, Lifestyle

Major modifiable risk factors for CAD

Age, male and post-menopausal women, family history

Non-modifiable CAD risk factors

Transient inability of coronary arteries to deliver enough oxygen to myocardial cells (supply-demand mismatch). Begins after 10 secs (cells can survive 20 mins)

Myocardial Ischemia

Times of increased O2 demand:

Exercise, tachycardia, HTN, valve disease

100

Times of decreaed O2 demand:

Coronary spasm, hypotension, dysrhythmia, anemia, hypoxia

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