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Unit 2 Objectives - Coggle Diagram

- - - - Normal Values mm Hg:
        
        CVP (preload): 1-5
        
        PAP: 17-32/ 4-13
        
        CO: 4-8 L/min (dec as ventricles fail)
        
        SABP: 90-140/ 60-80 (dec. in LVF)
        
        PCWP: 12-15 (Inc. in LVF)
        
        LVEF (stroke volume):
        lower than 40= LVF
      - CO = HR X SV
        incr preload = inc CO
        SV varies directly with preload and inversely with afterload
      - Preload: volume of blood returning to the heart- right atrial volume. volume of blood in the heart at the end of diastole
        CO: blood the heart pumps out of the LV each minute
        Afterload: Resistance that the ventricle must overcome to pump blood- aortic pressure
      - Which is a major determinant of diastolic blood pressure? Systemic vascular resistance
  - - - ECG: abnormalities, no specifics to heart failure
        Echo: size/fx/ structure of ventricles
        MGAS: dye injection, volume of ventricle contraction
        Catheterization/Angiography: hemodynamic monitoring, artery illumination
        Serum Electrolytes (hyponatremia, hypokalemia)
        Chest x ray (cardiomegaly = LVF)
        BNP testing = high >100 = heart failure
    - - Drugs:
        Aim to increase blood flow and O2
        
        Beta Blockers
        (Metoprolol, bisoprolol, atenolol) blocks SNS, cause lower HR, BP, lowers force of contraction, reduces O2 demand
        
        ACE inhibitors
        (Ramipril. captopril, lisinopril) blocks angiotensin II decreasing vasoconstriction, reduces sodium/ water retention, dilates arteries, reduces afterload, reduced O2 demand
        
        ARBs
        similar to ACE inhibitors,
        
        Aldosterone antagonist
        inhibits sodium, water retention, inhibits release of potassium, often results in hyperkalemia
        
        Diuretics
        reduce edema, often result in hypokalemia
        
        Inotropic Agents (Digoxin, dobutamine) incr. contraction force, slows HR, increased contractility
        
        Natriuretic
        induce diuresis
        
        Neprylisin Inhibitors
        prolonged natriuresis, however causes vasoconstriction
        
        Nitrates (or NTG)
        (NO) vasodilators, lower BP, increases coronary perfusion, reduces O2 demand
        
        dilates arteries (perfusion)
        
        reduces afterload / preload
        
        reduces O2 demand
        
        Calcium Channel Blockers
        reduced contractility, decreased O2 demand
      - Lifestyle:
        
        low-fat diet
        
        no smoking
        
        exercise
        
        low fluid, salt, cholesterol, alcohol
    - - Cholesterol = lipid that maintains cell membrane (normal up to 200 mg/dl)
        Comes from = animal fat and liver
        LDL = deposits cholesterol in tissues on artery walls
        HDL = takes cholesterol to liver for excretion, away from artery walls
    - - A group of symptoms that increase risk of coronary artery disease. Patients have 3X risk for atherosclerosis and stroke.
        
        apple shaped obesity
        
        glucose intolerance (>100 mg/mL)
        
        hyperinsulinemia
        
        decreased HDL
        
        hypertriglyceridemia
        
        hypertension (HTN)
    - - high lipids, glucose, nicotine, cholesterol
        
        endothelium is the primary site
        
        conditions such as hyperlipidemia, HTN, diabetes
  - - - Diagnosis Criteria:
        
        nocturnal dyspnea
        
        JVD
        
        lung crackles
        
        edema
        
        nocturnal cough
        
        exertion dyspnea
        
        pleural effusion
        
        reduced vital capacity
        
        tachycardia
        
        weight loss (4.5 kg or more)
      - S&S
        LVF (left for lungs)
        
        dyspnea
        
        cough
        
        orthopnea (lying flat)
        
        PND (dyspnea at night)
        
        weak pulses
        
        decreased perfusion, confusion, disorientation
        
        crackles
        
        pink frothy sputum
        
        RVF (right for rest of body)
        
        JVD
        
        Ascites
        
        GI disturbances
        
        reflux
        
        hepato-spleno-megaly
        
        peripheral edema
        
        pulmonary embolism
      - Four factors of heart failure:
        
        increased fluid volume
        
        impaired ventricular filling
        
        degeneration of ventricular muscle
        
        decreased ventricular contractile function
      - Causes:
        
        Ischemic Heart Disease- repeated insults to myocardium
        
        Chronic HTN- leading cause of LVF,
        
        Chronic pul. disease- leading cause of RVF
        
        Cardiomyopathy- myocardium injury
        
        Dysrhythmias
        
        Heart Valve (mitral regurgitation, atrial stenosis)
        
        Diabetes
        
        Multiple MIs
      - Pathophys::
        LVF:
        
        increased afterload- DIRECTLY AFFECTS CARDIAC OUTPUT*
        
        Hypertrophy
        
        decreased filling
        
        reduced SV and CO, arterial pressure
        
        decreased circulation results in feedback loop causing increased vasoconstriction & blood volume
        
        SNS stimulation = increased HR = more weakened heart
        
        RAAS stims = increased BP = more weakened heart
        -pulmonary edema
        
        RVF:
        
        causes hypoxemia
        
        forward contractile force is diminished
      - Treatments:
        
        aimed at reducing preload & afterload & increasing contractility
      - Early signs of cardiac problems in elderly:
        
        mental status changes
        
        agitation
        
        frequent falls
  - - - Risks:
        
        hypokalemia (from diuretic use)
        
        digoxin use
      - Supraventricular (SA node, atria, AV node)
      - Ventricular (bundle of His, Purkinje fibers, ventricular muscle)- potentially fatal
    - - tachy-dys: reduces time available for ventricular filling
        brady-dys: minimizes cardiac output, slows HR
        Atrial-dys: diminishes the volume emptied into the ventricle, decreasing SV
      - Premature ventricular contraction (PVC): when ectopic pacemaker initiates a contraction. Beats without waiting for completion of each action potential. Leads to fibrillation, rapid heart beat, quivering ventricle, no blood ejecting.
  - - - Severe Hypovolemic Shock
        
        large depletion of blood or fluids.
        low blood pressure, reduced blood flow,
        RAAS is activated, vasoconstriction occurs,
        Causes SNS stimulation, increased HR and contractility. .
      - Cardiovascular shock
        
        Caused by heart failure and severe MI or cardiac tamponade
        Causes severe HTN and tachycardia, decreased renal perfusion
        cold, clammy skin, decreased BP (below 90 mm Hg systolic), increased HR, change of consciousness
        loss of perfusion in arteries, low urine output, cyanosis, SNS and RAAS is stimulated causing vasoconstriction
  - - - HTN: Aging adults require higher BP for organ circulation (150/90). Risk factors include diabetes, obesity, sedentary behavior, tobacco, excess sodium, low potassium, low vitamin D, excess alcohol, stress. Causes damage to arteries and resistance against left ventricle. Results in muscle hypertrophy, ischemia, infarction, and heart failure
      - Atherosclerosis: primarily located in tunica intima, Risk factors: Men, Old, Diabetes, African American, Genetic disposition, Tobacco, HTN, Obesity, high fat diet, high stress,
      - Varicose Veins: caused by high pressure in veins, damaging valves, prolonged standing, sitting, pregnancy, obesity. Effects include edema of legs
        DVT: DV insufficiency causes edema, heaviness of leg, dusky color of leg. Result from incomplete clearance of waste, accumulation of CO2, lactic acid. Leads to DVT, a clot that moves to the IVC then the right side of the heart into pulmonary artery. Risk factors include Virchow's triad, venous stasis, hypercoagulability, vascular damage. Signs include tenderness, redness, warmth, swelling.
        Thrombophlebitis: inflammation preceding clot
        Phlebothrombosis: clot, unassociated with inflammation
- - - - Compensatory Mechanisms
        
        Likewise, in conditions in which pH is too high, the kidneys reabsorb more H+ and excrete more HCO3, thereby lowering the pH, compensating for alkalosis. .
        
        The kidneys’ compensation is slow and may take days to reach maximal effectiveness
        
        In conditions in which pH is too low, or acidic, the kidneys excrete more acid (H+) and reabsorb more base (HCO3−). These actions lessen the amount of acid in the blood while adding more base (HCO3−), thereby raising blood pH and compensating for acidosis.
      - Medical Intervention
        
        Acidosis: administer sodium bicarb, intubate/ mechanical ventilation
        
        Alkalosis: CO2 rebreather mask to increase CO2
    - - Medical Intervention
        
        Acidosis: administer sodium bicarb, give insulin in Diabetic Ketoacidosis (DKA)
        
        Alkalosis: administer Acetazolamide (increase bicarb excretion), antiemetic meds when vomiting
      - Compensatory Mechanisms
        
        In conditions in which pH is too low, or acidic, the lungs increase breathing to expel CO2 (hyperventilation).
        When pH is high, the lungs slow breathing to retain CO2 (hypoventilation)
        
        The lungs are fast to react
- - - - Cough, dyspnea, hemoptysis, atelectasis. hypoxia, respiratory failure (pulmonary edema, PE, pneumonia, pneumothorax)
      - Hypercapnia, hypoxia, pulmonary HTN,
    - - Upper
        
        one of the more frequent reasons to seek care
        includes nose, oropharynx, larynx, trachea, and two main bronchi/ bronchioles
        
        conducts air into the lower airways
        
        Mucociliary apparatus: inside the bronchioles, secrete mucus that traps foreign organisms and protects the lower respiratory system
        
        Rhinitis, Pharyngitis, Sinusitis, Tonsillitis, Epiglottitis, Laryngitis, Tracheitis,
      - Lower
        
        gas exchange by oxygenating blood and excreting CO2 at the alveoli
        
        Bronchitis, Pneumonia, Abscess, Tuberculosis,
    - - viruses alter the pulmonary immune defenses making the lungs vulnerable to bacterial infection. Common culprits causing secondary infections are influenza, rhinovirus, syncytial virus
    - - Causes: commonly strep and staph bacteria
        Treatment: anti-fungal,
      - Community Acquired: obtained outside hospital setting,
      - Side Effects: pleuritic chest pain, crackles, cough with sputum, tachycardia, dyspnea, rigors, fever, chills,
        consciousness changes and low/normal temp with older adults
    - - characterized by diffuse alveolar injury, capillary damage, pulmonary infiltrates, and severe hypoxemia
      - causes include multisystem organ failure, sepsis, aspiration of gastric contents, systemic illnesses, and injuries
        death often results as treatments are ineffective
      - Signs include sudden pulmonary edema, severe hypoxemia, and hypercapnia. Hypoxemia does not improve with oxygen.
    - - a consequence of LEFT SIDED HEART FAILURE
      - Creates a fluid barrier to oxygen transfer across the alveoli-capillary interface
      - Symptoms: Hypoxia, crackles in lungs, NO FEVER
    - - radon gas, smoking, second hand smoke, chemical agents, asbestosis, silicosis
    - - signs: diminished gag or cough reflex, decreased level of consciousness
      - results can range from no injury to death
        small quantities is common, and can be coughed out
        those with underlying disease are at greater risk
      - more common in the right lung- due to the right bronchus being vertical and wider than the left bronchus
  - - - Right sided heart failure:
        
        hypoxemia, hypercapnia, edema
        elevated PVR --> HTN
        
        Ascites, dyspnea, hepatosplenomegaly, anorexia, dependent edema, pink frothy sputum, distended jugular veins,
      - Chronic hypoxia
        
        requires oxygen therapy
      - Emphysema and chronic bronchitis (see Coggle)
    - - Caused by compressive force on the alveoli, such as a mass, obstruction of bronchioles, complications post surgery due to sedation,
      - Results in collapse of alveoli and reduced gas exchange, Predisposes patient to pneumonia.
      - To relieve it, coughing and deep breathing are recommended
    - - Chronic
        
        airway stays small. chronic inflammation and tissue remodeling
      - Acute
        
        hypersensitivity reaction: bronchospasm. edema. airway obstruction
      - Mode of action: Triggers (irritants, infections, others) --> mediator release (histamine, leukotriene, cytokines --> hyperactive response and chronic responses
    - - obstructive
        
        trouble exhaling air from lungs; difficult to inhale fresh air. The old air obstructs the new air
        
        increase in resistance to airflow from the trachea and larger bronchi to respiratory bronchioles
        
        emphysema, chronic bronchitis, bronchiectasis, and asthma
      - restrictive
        
        trouble fully expanding their lungs. Difficult to fill their lungs with air. Lungs are restricted from normal breathing.
        
        reduced expansion of lung tissue and decreased total lung capacity (TLC)
        
        hypersensitivity pneumonitis, pulmonary fibrosis, pneumoconiosis, and thoracic cage deformities