Cardiovascular Function and Diseases Flashcards
Heart wall (inner to outer)
- Endocardium
- Myocardium
- Epicardium (or visceral pericardium)
- Pericardial cavity
- Parietal pericardium
Endocardium
Innermost layer
Myocardium
Thickest layer of cardiac muscle
Cardiac myocytes (muscle cells) provide contractile force to propel blood
Epicardium
Inner layer of the pericardium that lies against the heart surface
Also called visceral pericardium
Parietal pericardium
Outer layer of the pericardium that is in contact with lungs and the structures in the chest cavity
Pericardial cavity
Space between the visceral and parietal pericardium layers
Contains pericardial fluid (approx. 20 ml)
Functions:
- Prevents displacement of heart during movement
- Protects heart from infection/inflammation from lungs and other surrounding tissue
- Contains receptors that can control HR and BP
Heart chambers
RA
RV
LA
LV
Atria are smaller and thin-walled; “storage units” and passageways to the ventricles
Ventricles are larger and thick-walled; pumping chambers
Atrioventricular valves (AV)
In-between each atria and ventricle:
- Right AV valve: tricuspid valve (TV)
- Left AV valve: mitral valve (MV)
Function as a unit to simultaneously allow blood flow from atria into ventricle, and prevent back flow into atria from ventricle when the ventricle contracts
Semilunar valve (SV)
In-between RV and pulmonary artery, and LV and aorta
Open to allow blood to flow from ventricles into greater vessels, and close to prevent back flow into ventricles
Coronary arteries
Supply myocardium and other heart structures with oxygenated blood
Originate from the aorta, and divide into smaller RCA and LCA branches
Coronary veins
Coronary sinus: empty deoxygenated blood from heart into the RA
Cardiac cycle
One heartbeat accounts for one contraction (systole) and one relaxation (diastole)
Systole: contraction (blood leaves the ventricles)
Diastole: relaxation (ventricles fill)
Cardiac conduction
- SA node (“pacemaker” of the heart), located at junction of RA and SVC, generates action potential (AP; 60-100/min)
- Atria contract
- AP travels through myocardium to the atrioventricular (AV) node where they pass to the ventricles
- Bundle of His, located in the interventricular septum, divides into right and left bundles which conduct impulses to the ventricular apex
- Purkinje fibers are the end branches of the bundles
- Ventricles contract
Myocardial AP
Depolarization: electrical activation of muscle cells
Repolarization: deactivation of muscle cells
Caused by movement of ions (Na2+, Ca+, K+, Cl-) across the cardiac cell membrane that results in a voltage difference (membrane potential)
AP phases
Phase 0: depolarization (rapid Na+ entry into cell) (+30 mV)
Phase 1: early repolarization (slow Ca2+ entry into cell)
Phase 2: plateau; continued repolarization (slow Na+ and Ca2+ entry into cell)
Phase 3: late repolarization (K+ moves OUT of cell)
Phase 4: return to resting membrane potential (-70 mV)
PQRST EKG wave
P-wave: atrial depolarization
QRS complex: ventricular depolarization and atrial repolarization
T-wave: ventricular repolarization
Myocytes (cardiac cells)
Characteristics:
1. Intercalated disks with gap junctions allow electrical impulses to spread quickly from cell to cell
- More mitochondria due to increased ATP need
- Increased T-tubules (invagination of muscle membrane) allow faster access to Na+ and K+; conduct impulse to sarcoplasmic reticulum (smooth ER within myocytes) that store Ca2+
Atherosclerosis
Chronic inflammatory condition characterized as thickening and hardening of vessels
Characteristics:
- Endothelial (blood vessel lining) dysfunction
- Plaque development/narrowing, and/or instability
Consequences (vascular events): MI, stroke, renal artery disease, aneurysm, PAD, CAD
Development of atherosclerosis
- Chronic endothelial injury
- Immune response adheres to injury
- Inflammatory response
- LDL cholesterol penetrates vessel wall and becomes trapped
- Macrophages with lipids inside accumulate and form a “fatty streak” that release inflammatory cytokines
- Cytokines stimulate vessel smooth muscle growth
- Plaque forms over the fatty streak
- Plaque can calcify and obstruct blood flow, OR rupture (a “complicated plaque”)
- Plaque rupture exposes vessel underneath, and thrombus forms rapidly, which can obstruct the vessel (angina, infarction)
Lipids
Necessary for life (cell membranes, hormone development, bile production)
Types of lipids:
1. Chylomicrons: consist mostly of triglycerides; transport dietary fat from intestine to liver and peripheral cells
- Triglyceride: major form of lipid; used for energy
- Very Low Density Lipoproteins (VLDL): triglycerides and protein
- LDL (“Bad”): cholesterol and protein; delivers cholesterol from liver to cells (cell membranes, steroid hormones)
- HDL (“Good”): phospholipid and protein; returns excess cholesterol from cells/artery walls to liver to be converted to bile salts
Risk of CAD (r/t dyslipidemia)
Linked to:
1. High triglycerides, VLDL, and LDL
- Low HDL
HTN
Consistent, sustained elevation of BP >130 mmHg systolic OR >80 mmHg diastolic
Increases risk of atherosclerotic disease and MI
BP classification
Normal: <120/<80
Elevated: 120-129/<80
HTN Stage 1: 130-139/80-89
HTN Stage 2: >140/>90
Goal for BP in pts with diabetes and/or renal disease is <130/80 (below HTN stage 1)
Primary HTN (95% of cases)
HTN that is NOT related to another disorder
Risks: FHX, age, gender, ethnicity, high dietary sodium, glucose intolerance, tobacco, obesity, heavy alcohol consumption, low dietary intake of Ca2+, K+, and Mg2+
Sympathetic Nervous System (SNS) and HTN
Normally, the SNS promotes maintenance of BP and tissue perfusion
SNS over-activity in pts with HTN can result in excess production and secretion of (1) catecholamines (epinephrine or norepinephrine) OR (2) insulin
Catecholamines increase HR, BP, RR, muscle strength, and mental alertness
Insulin increases sodium and water reabsorption (thus increases BP, ECF)
RAAS and HTN
Normally, RAAS promotes maintenance of BP and tissue perfusion
RAAS over-activity can result in excess secretion of renin, angiotensin II, and aldosterone which (1) increase blood vessel tone (vasoconstriction) and (2) promote salt and water retention
Secondary HTN (5% of cases)
HTN caused by an underlying disease process
Caused by: Renal, endocrine and vascular systemic diseases, pregnancy, neurologic disorders, acute stress, medications, and substances
Ex.: Renal failure, pheochromocytoma (tumor on adrenal gland that secretes excess catecholamines), arteriosclerosis, and increased ICP (intra-cranial pressure)
Other types of HTN
Complicated HTN: damages the walls of systemic blood vessels
Malignant HTN: rapidly progressive HTN (crisis) in which the diastolic BP is usually >140 mmHg
Orthostatic HYPOtension: decrease in BP >20 mmHg systolic OR >10 mmHg diastolic within 3 minute of moving to a standing position
Aneurysm
Localized enlargement/dilation of an artery caused by a weakened artery wall or cardiac chamber
Types of aneurysm:
1. True aneurysm: involves distention of all 3 layers of the artery wall
- False aneurysm: leaking of the vessel forming a clot outside the vessel wall (hematoma)
Varicose veins
Vein in which blood has pooled causing distortion, tortuous, and inflammation of the vein (palpable; usually in the saphenous vein)
Caused by: Trauma or gradual venous distention, rendering valves incompetent
High risk for developing clots
Chronic venous insufficiency
Inadequate venous return over a long period as a result of varicose veins and/or valve incompetence
S/S: Pain, swelling, skin discoloration (darkening), venous stasis ulcers
Increased risk for infection and clotting d/t poor circulation
Deep Venous Thrombosis (DVT)
Thrombosis: clot (usually in a large vessel; saphenous vein)
Thromboembolism: detached thrombus (that can lead to PE)
Veinous flow obstruction leads to increased venous pressure and post-thrombotic syndrome (characterized by pain, swelling, ulceration of affected limb)
DVT management depends on clot formation risk and detachment (embolus)
DVT risk factors (Virchow’s Triad)
- Venous stasis
- Venous endothelial damage
- Hyper-coagulable states (Smoking, liver disease, CA, pregnancy)
CAD
Any vascular disorder that narrows or occludes the coronary arteries, resulting in an imbalance between supply of blood and myocardial demand for oxygen and nutrients
Reversible myocardial ischemia or irreversible MI may result
Most common cause: Atherosclerosis
Non-modifiable risk factors: Age, FHX, males, post-menopause women
Modifiable risk factors: Dyslipidemia, HTN, smoking, DM and insulin resistance, obesity, diet
Nontraditional risk factors: Markers of inflammation and thrombosis (C-reactive protein, troponin I, hypergomocysteinemia), adipokines, infection (microorganisms and periodontal disease), air pollution, coronary artery calcification
Acute Coronary Syndrome
Sudden coronary artery obstruction because of thrombosis formation over a ruptured atherosclerotic plaque
Ex.: Unstable angina, MI
Most common complications: Dysrhythmias, CHF, sudden death
Myocardial ischemia
Supply of coronary blood does not meet the demand of the myocardium for oxygen and nutrients
S/S:
Stable angina: predictable chest pain; caused by (expected by): physical exertion, stress; lasts a short-time, DOES NOT change frequency/worsen over time; relieved by rest/medication
Prinzmetal (varient) angina: un-predictable chest pain
Silent ischemia: causes no detectable symptoms
Angina pectoris: transient substernal chest discomfort
Unstable angina
A form of reversible myocardial ischemia; indicates that a plaque has ruptured and MI may occur soon; EMERGENCY
Unpredictable; occurs at rest, and may occur with exertion/stress; NOT relieved by rest/medicine
Types of unstable angina:
1. Rest angina: occurs at rest; usually prolonged >20 min
- New-onset angina: new and symptomatic with everyday activities
- Increasing angina: previously diagnosed, but become more frequent/longer duration, and/or increased with less activity
Myocardial Infarction (MI)
Prolonged myocardial ischemia that causes irreversible damage
ST segment elevation (STEMI) requires immediate intervention (cathlab); smaller infarction (NSTEMI) suggests additional myocardium is still at risk for recurrent ischemia and MI
Two major types of MI:
1. Subendocardial MI: LESS of the myocardium
- Transmural MI: through the WHOLE wall of the myocardium
CV system: Fetus developmental anatomy
Cardiogenesis begins at approx. 3 weeks’ gestation
- Heart arises from the mesenchyme
- Heart develops as an enlarged blood vessel with a large lumen and muscular wall; midsection grows faster than the ends (week 5)
- Heart tube elongates and rotates to the right (bulboventricular loop); fetal heart contractions begin (week 7)
- All fetal heart and vascular systems present (week 8)
In-Utero: Fetal shunts
Foramen ovale: opening between the atria
Ductus arteriosus: connects pulmonary artery to the aorta (bypasses underdeveloped lungs)
Ductus venosus: connects umbilical vein to the IVC (bypass underdeveloped liver)
Fetal circulation
- LA
- LV
- Aorta
- Systemic circulation
- Umbilical arteries
- Placenta
- Umbilical veins
- Ductus venosus (bypass liver)
- IVC
- RA
- (1) RV; (2) Foramen ovale
- (1) Pulmonary artery; (2) LA
- (1) Ductus arteriosus (bypass lungs); (2) LV
- Aorta
Transitional circulation
Circulatory changes take place after birth (gas exchange shifts from placenta to lungs)
Fetal shunts close
Congenital heart defects
It is the leading cause of death (except for prematurity) in 1st year of life
Cause of defect known in only 10% of cases
Risk factors: Prenatal (maternal rubella, insulin-dependent diabetes, alcoholism, PKU, hypercalcemia), environmental, and genetic (chromosomal aberrations)
Types of defects:
1. Patent ductus arteriosus (PDA): ductus arteriosus fails to close after birth; allows a portion of oxygenated blood to back flow directly from the aorta to the lungs and pulmonary (pulmonary HTN)
- Atrial septal defect: abnormal opening between the atria after birth
- Ventricular septal defect (VSD): abnormal opening between the ventricles after birth; common (25-33% of cases)
Other defects: Coarctation (congenital narrowing) of the aorta, aortic valve stenosis, pulmonary artery/valve stenosis, and hypoplastic left heart syndrome (underdevelopment)
Tetralogy of Fallot
Syndrome represented by four defects:
- VSD
- Overriding aorta straddles the VSD (allows deoxygenated blood from RV to enter aorta)
- Pulmonary stenosis
- RV hypertrophy
S/S: Cyanosis, clubbing, feeding difficulty, and squatting (attempt to force more blood into heart and the narrow area of the pulmonary artery)
Hypercyanotic spell (“tet spell”) generally occurs with crying and exertion
Most causes corrected surgically in early infancy before first year of age (reestablishes reliable pulmonary blood flow)
HTN in children
Children often have underlying renal disease or coarctation (congenital narrowing) of the aorta; cause of HTN is almost always found; commonly asymptomatic
Clinical manifestation: Systolic and diastolic BP >95th percentile for age and gender on at least 3 occasions
Tx: Diet, regular physical activity, avoidance of smoking and drugs
