Week 4 - Cardiovascular System

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Week 4 - Cardiovascular System
2013-07-23 19:43:11

Function and Dysfunction of Cardiovascular system
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  1. Normal Cardiovascular system
    • Anatomy: closed loop, systemic circulation, pulmonary circulation
    • Arterial system
    • Capillary system
    • Venous system
    • Lymphatic system
  2. Lymphatics
    • Collect fluids that leak out of the arteriole/capillary circuit under high hydrostatic pressure and return it to lymphatic channels
    • -system of 1-way valves
    • -Pass through lymph nodes
    • -swelling: obstruction or infection
  3. Lymphedema
    • Normal flow of lymph is blocked or altered.
    • Lymph collects in the interstitium: inflammation
    • Not much we can do about this; best treatment is through occupational therapists and PTs to work on to get fluid to return to vascular system
  4. Control of Heart Rate
    • Intrinsic: SA, automaticity, rhythmicity
    • Local mediators: baroreceptors (sense pressure) & chemoreceptors (chemcials)
    • Nervous (autonomic): Sympathetic (turn up <3 rate) and parasympathetic (turn down <3 rate) nerves
  5. Inotropy
    strength of heart contraction
  6. Chronotropy
    heart rate
  7. Dromatropy
    conduction of heart
  8. Stenosis (valvular disease)
    • Failure of valve to open completely
    • Develops a pressure gradient across the valve
    • -normally pressure is 0 mmHg 
    • -Stenosed valve 6-8 mmHg pressure gradient (blood must force through high resistance of the narrow opening)
    • *Hypertrophy occurs as compensatory mechanism
  9. Regurgitation
    • Insufficiency (opposite of stenosis) 
    • Failure of valve to close completely
    • Allows blood to leak back/flow in reverse
    • Increases heart's workload
  10. Mitral stenosis
    • Mitral Valve Disease of LEFT HEART
    • Atrial pressure > ventricular pressure
    • Thickening of L atrium -> chamber enlarges -> hypertrophy -> ↑ pul. vasc. pressure -> chronic pul HTN -> R ventricle hypertrophy -> R heart failure
    • Pulmonary congestion
    • Diastolic murmur
  11. Mitral regurgitation
    • Mitral valve disease (Left heart)
    • Backflow from L ventricle into L atrium:
    • -both dilate, hypertrophy
    • -increased afterload increases the regurgitation
    • -If not fixed, leads to L heart failure
    • Systolic murmur (backflow during L ventricle contraction)
  12. Preload
    The volume and associated pressure generated in the ventricle at the end of diastole (before contraction)
  13. Mitral valve prolapse (MVP)
    • mitral valve balloons up into the L atrium
    • valve is "floppy" and doesn't close tightly
  14. Aortic stenosis
    • Due to age-related calcification
    • Obstruction of aortic outflow from L ventricle (systole) 
    • L ventricle hypertrophies and ↑ afterload leads to L HF and pulmonary compliations
    • Systolic murmur (when L ventricle contracts)
  15. Aortic regurgitation
    • blood leaks back into L ventricle from aorta
    • L ventricle volume overload --> hypertrophy, dilation, ↑ systolic BP 
    • Left HF from increased workload
    • High-pitched blowing murmur during diastole
  16. Infective Endocarditis (IE)
    • Infection and inflammation of the endocardium, especially the cardiac valves
    • Bacteria most common cause (Streptococci, staphylococci)
    • -bacterial adherence -> fibrin and thrombus formation (Bad!)
    • Risk: history of rheumatic heart disease, congenital disease, prosthetic valves (bacteria like to sit on these), valvular heart disease, trauma (procedure)
    • S/S: fever, new or changed heart murmur, petechial lesions, chest pain
    • Physical findings specific to endocarditis: 
    • -janeway lesions (usually nonpainful and on hands)
    • -Osler nodes (painful, block flow, can eat away tissue)
    • Complications: HF, systemic spread of microemboli (everywhere.. can lodge in kidney and cause kidney failure)
  17. Acute pericarditis
    • acute inflammation of the pericardium
    • idiopathic (unknown) or viral most common
    • membranes inflamed and roughened
    • A pericardial effusion may develop (buildup of fluid.. up to 2 L!)
    • S/S: fever, chest pain, SOB (pt usually sits forward to relieve SOB)
    • Complications: effusion (small ones will usually reabsorb), constriction, tamponade (acute type of pericardial effusion
  18. Cardiac Tamponade
    • buildup of blood or fluid in the pericardial sac, putting pressure on the heart which can prevent it from pumping effectively. 
    • systemic venous congestion
    • Treatment: pericardiocentesis
    • Emergency!!
  19. Shock
    • Widespread impairment of cellular metabolism
    • Many causes and manifestations
    • Progresses to organ failure if not treated!!
    • Syndrome.. when cells are not receiving or cannot use oxygen
  20. Compensatory mechanisms in SHOCK
    • Homeostatic mechanisms maintain adequate tissue perfusion despite reduction in CO: RAAS, baroreceptors (signal to brain to turn up <3 rate)
    • SNS activation: tries to maintain BP even though CO has fallen by temporarily increasing venous return to heart by: 
    • -E/NE: B1 stimulation to ↑ HR, vasoconstriction
    • -gastric vessels constrict
    • -urine output = 0 to conserve fluid --> renal damage (ARF)
  21. Cardiogenic shock
    • Heart muscle is damaged and contractility is impaired, usually from MI, cardiomyopathy
    • HypOtension, cool, clammy skin, altered mentation reduced urine output, metabolic acidosis, pulmonary edema
    • GOAL: improve CO and myocardial O2 delivery (<3 transplant, VAD, Intra-aortic balloon pump [IABP])
  22. Hypovolemic shock
    • Inadequate circulation of blood volume
    • -dehydration
    • -hemorrhage 
    • -3rd spacing: loss of volume in intracellular, vascular, and interstitial spaces
    • Cool, clammy skin, tachycardia, delayed capillary refill, decreased urinary output, thirst, thready pulse
    • GOAL: stop bleeding and replace fluid/blood
  23. Neurogenic
    • AKA 'vasogenic' shock
    • massive, widespread vasodilation of PNS overstimulation and SNS understimulation
    • Caused by spinal cord or medulla trauma
    • Causes a "relative hypovolemia"
    • GOAL: return fluids and vasoconstriction
    • Low HR and BP, blood pooling in extremities,
  24. Anaphylactic
    • Widespread hypersensitivity reaction 
    • Leaky vessels and massive vasodilation from histamine release
    • Treat with Epinephrines and histamine blockers (to stop dilation)
  25. Septic Shock
    • Form of distributive shock
    • Severe systemic inflammatory response to infection, characterized by release of immune mediators
    • Common causes: Gram - and + bacteria, fungal infections, endotoxins
    • Clotting cascade, complement system, and kinin system are activated 
    • Widespread inflammation leads to profound peripheral vasodilation w/ hypOtension, maldistribution of blood flow w/ cellular hypoxia, and increased permeability w/ edema formation
    • Complications: ARDS, DIC
  26. Acute Respiratory Distress Syndrome (ARDS)
    • Most commonly associated with septic shock
    • Neutrophils release proteolytic enzymes, produce oxygen-free radicals, and secrete inflammatory chemicals that make pulmonary capillaries leak
    • -Inflammation of the lung parenchyma leads to impaired gas exchange with systemic release of inflammatory mediators, causing inflammation, hypoxemia and frequently multiple organ failure.
    • -Has a 90% death rate in untreated patients. With treatment, usually mechanical ventilation in an ICU, the death rate is 50%
  27. Disseminated Intravascular Coagulopathy (DIC)
    • Immune activation of clotting cascade
    • -leads to the formation of small blood clots inside the blood vessels throughout the body
    • -small clots consume coagulation proteins and platelets
    • -normal coagulation is disrupted and abnormal bleeding occurs from the skin, GI tract, respiratory tract and surgical wounds
    • -The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result
  28. Acute Renal Failure (ARF)
    • Complication of all types of SHOCK
    • Kidneys undergo long periods of hypoperfusion
    • -vasoconstriction causes decreased glomerular blood flow
    • -OR-
    • -Acute tubular necrosis (ATN) associated decreased urinary excretion of waste products --> intrarenal failure
  29. Multiple Organ Dysfunction Syndrome (MODS)
    • Most common causes: sepsis and septic shock
    • Initiated by immune mechanisms that are overactive and destructive
    • Cytokines affect endothelium, recruit neutrophils, and activate inflammation in
    • vascular beds leading to tissue destruction and organ dysfunction
    • *We can often recover for this, but once organs start to shut down, DOWNHILL -> mortality ↑
  30. Embryonic heart (Congenital HD, heart disease)
    • Lungs are collapsed in human fetus
    • 2 passageways in embryonic heart permit blood flow to bypass the lungs 
    • -Foramen ovale: Flow is RA -> LA (blood bypasses pulmonary circulation and no O2!)
    • -Ductus Arteriosus: Connects pulmonary artery and aorta; Flow is Pulm art -> Aorta (can cause no symptoms or heart murmur, etc.)
    • *Foramen and ductus usually close shortly after birth.
  31. Right to Left Shunt
    • Allows unoxygenated blood from the R heart to enter the L heart and systemic circulation w/o passing through the lungs first
    • -Leads to cyanosis and ↓ PaO2 (arterial partial pressure of O2 - tissue oxygenation)
  32. Left to Right Shunt
    • Allows oxygenated blood from the L heart (aorta) to enter the R side
    • -No cyanosis b/c recirculated through lungs
    • -Over time leads to R ventricular hypertrophy due to increased pressure in R heart
  33. Acyanotic Defects
    • Atrial-septal defect (ASD): Foramen ovale stays open to some degree
    • Ventricular-septal defect (VSD)Most common; L>R pressure after birth leads to R heart failure.
    • Coarctation of the Aorta: Narrowing/stricture impedes blood flow
    • Patent Ductus Arteriosus (PDA): The pulmonary artery (deox. O2) remains connected to aorta (ox. O2)
    • *All are Acyanotic b/c L>R, so oxygenated blood wins
  34. Cyanotic Defects: Tetralogy of Fallot (TOF)
    • A congenital heart defect which involves four anatomical abnormalities of the heart:
    • 1) Ventricular-septal defect (VSD)
    • 2) Over-riding Aorta: aorta positioned above VSD opening
    • 3) Pulmonary stenosis: obstructs R ventricular outflow
    • 4) R ventricular hypertrophy
    • *TOF is the most common cause of blue baby syndrome.
    • Cyanosis occurs from overriding aorta that receives deoxygenated blood
  35. Cyanotic Defects: Transposition of the Great Arteries
    • Aorta arises from the R ventricle and pulmonary artery arises from the L ventricle (opposite from normal)
    • 2 separate but non-communicating circulations
    • Fatal unless septal defects are also present
  36. Atherosclerosis
    • Thickening and hardening of arterial wall
    • Begins w/ injury to endothelial cells that line artery walls
    • inflammation -> accumulation of lipid-laden macrophages -> formation of plaque
    • Hyperlipidemia is the major cause/risk factor in development
    • Consequences: angina pectoris, CHF
  37. Angina Pectoris
    • Supply-demand problem: myocardial ischemia w/o cell death (cells are hungry for O2 but haven't died yet) 
    • Higher demand for O2 than supply
    • Myocardium has little tolerance for hypoxia: cardiac cells go into anaerobic metabolism and are viable for only 20 mins under ischemic conditions
    • S/S: substernal chest pain that can radiate to jaw or left arm, squeezing sensation, EKG changes, usually brought on by physical activity & subsides w/ rest.
    • *Atypical symptoms!* -> Often hard to tell and catch b/c large portion of population will not express symptoms above!**
  38. Myocardial Ischemia
    • Angina: O2 supply is not adequate to meet demands
    • Stable: predictable and can take medicine ahead of time.
    • Unstable: unpredictable from thrombus movement
    • Prinzmetal's Angina (Variant): unpredictable, often at rest, vasospasm, night chest pain, > in women, coronary artery vasospasm (seems like <3 attack but not from blockage but from spasms.
  39. Myocardial Infarction (MI)
    • prolonged ischemia causing irreversible damage to heart muscle
    • Heart attack!! Cells die and form scar tissue
    • Mostly caused by thrombotic occlusion
    • 2 types:
    • -Non ST elevation MI (N-STEMI)
    • -ST elevation MI (STEMI)
    • Clinical manifestations: prolonged chest pain, progresses, pallor, cyanosis, SOB, diaphoresis, nausea, radiating pain, BP changes, crackles in lungs, EKG changes
    • Complications: changes in electrical currents, dysrhythmias, thromboemboli, sudden death, myocardial rupture, pericarditis, organ failure
  40. Acute Coronary Syndrome (ACS)
    • Form of MI
    • Time is MUSCLE! #1 rxn to chest pain is denial
    • *Educate patients to call ambulance!!*
    • Irreversible cell injury after occlusion happens after 20 minutes
    • Necrotic tissue: replaced by 6 weeks by tough fibrous scar tissue
  41. Heart Failure (HF)
    • heart cannot meet metabolic and/or O2 demands - insufficient pump
    • impaired systole or diastole or both
    • Not a disease, a syndrome
    • L or R heart failure
    • Limitations to compensation: 
    • -Frank-Sterling: heart cannot pump the extra blood and heart stretches and enlarges
    • -RAA activation: adds to blood volume and diastolic preload, making things worse! Also vasoconstriction, ↑ BP
    • -Hypertrophy: increased stress, myocardial cells increase in size, not number, EF (ejection fraction) and CO ↓
  42. Types of Failure
    • R-sided:
    • -pulmonary stenosis or HTN
    • -R ventricular MI
    • -pulmonary embolism
    • -cor pulmonale (failure of the R side of the heart brought on by long-term high blood pressure in the pulmonary arteries and right ventricle of the heart)
    • *Pulmonary disorders; backward (congestion in systemic venous system - hepatomegaly, ascites, splenomegaly, anorexia, edema, jugular vein distensions); forward (Low output to L vent leading to low CO - fatigue, oliguria, ↑ HR, faint pulses, confusion, anxiety)

    • L-side:
    • -aortic stenosis
    • -L vent MI
    • -HTN
    • -Mitral stenosis
    • *Most associated with: backward effects (accumulation of blood in pulmonary circulation - dyspnea, orthopnea, cough, cyanosis, crackles) & forward (same as R-side)
  43. Cardiomyopathy (CM)
    • Dilated/Congestive (DCM)
    • -all 4 chambers dilated & weak,