MAP = CO × SVR, CI = CO/BSA

  Kidney gets 25% of CO, brain gets 15%, heart gets 5%

  Preload – left ventricular end-diastolic length, linearly related to left ventricular end-diastolic volume (LVEDV) and filling pressure

  Afterload – resistance against the ventricle contracting (SVR)

  Stroke volume determined by LVEDV, contractility, and afterload

•  Stroke volume = LVEDV – LVESV

  Ejection fraction = stroke volume/LVEDV

  EDV (end-diastolic volume) – determined by preload and distensibility of the ventricle

  ESV (end-systolic volume) – determined by contractility and afterload

  Cardiac output increases with HR up to 120–150 beats/min, then starts to go down because of decreased diastolic filling time

  Atrial kick – accounts for 20% of LVEDV

  Anrep effect – automatic increase in contractility secondary to ↑ afterload

  Bowditch effect – automatic increase in contractility secondary to ↑ HR

  Arterial O₂ content (CaO₂) = Hgb × 1.34 × O₂ saturation + (Po₂ × 0.003)

  O₂ delivery = CO × arterial O₂ content (CaO₂) × 10

  O₂ consumption (VO₂) = CO × (CaO₂ – CvO₂); CvO₂ = venous O₂ content

•  Normal O₂ delivery-to-consumption ratio is 5:1. CO increases to keep this ratio constant.

•  O₂ consumption is usually supply independent (consumption does not change until low levels of delivery are reached)

  Causes of right shift on oxygen–Hgb dissociation curve (O₂ unloading) – ↑ CO₂, ↑ temperature, ↑ ATP production, ↑ 2,3-DPG production, or ↓ pH

•  Opposite above causes left shift (increased O₂ binding)

•  Normal p50 (O₂ at which 50% of O₂ receptors are saturated) = 27 mm Hg

  ↑ SvO₂ (saturation of venous blood, normally 75% ± 5%; used on some Swan–Ganz catheters) – occurs with ↑ shunting of blood or ↓ O₂ extraction (eg sepsis, cirrhosis, cyanide toxicity, hyperbaric O₂, hypothermia, paralysis, coma, sedation)

  ↓ SvO₂ – occurs with ↑ O₂ extraction or ↓ O₂ delivery (eg ↓ O₂ saturation, ↓ CO, malignant hyperthermia)

  Wedge – may be thrown off by pulmonary hypertension, aortic regurgitation, mitral stenosis, mitral regurgitation, high PEEP, poor LV compliance

  Swan–Ganz catheter – should be placed in zone III (lower lung)

•  Hemoptysis after flushing Swan–Ganz catheter – increase PEEP, which will tamponade the pulmonary artery bleed, mainstem intubate non-affected side; can try to place Fogarty balloon down mainstem on affected side; may need thoracotomy and lobectomy

•  Relative contraindications – previous pneumonectomy, left bundle branch block

•  Approximate Swan–Ganz catheter distances to wedge – R SCV 45 cm, R IJ 50 cm, L SCV 55 cm, L IJ 60 cm

•  Pulmonary vascular resistance (PVR) can be measured only by using a Swan–Ganz catheter (ECHO does not measure PVR)

•  Wedge pressure measurements should be taken at end-expiration (for both ventilated and nonventilated patients)

  ↑ Ventricular wall tension (#1) and HR are the primary determinants of myocardial O₂ consumption → can lead to myocardial ischemia

  Unsaturated bronchial blood – empties into pulmonary veins; thus, LV blood is 5 mm Hg (PO₂) lower than pulmonary capillaries

  Alveolar–arterial gradient – is 10–15 mm Hg in a normal nonventilated patient

  Blood with the lowest venous saturation → coronary sinus blood (30%)

SHOCK

  Shock = inadequate tissue oxygenation (most basic definition)

•  Tachypnea and mental status changes occur with progressive shock

  Adrenal insufficiency

•  MCC – withdrawal of exogenous steroids

•  Acute – cardiovascular collapse; characteristically unresponsive to fluids and pressors; nausea and vomiting, abdominal pain, fever, lethargy, ↓ glucose, ↑ K

•  Tx: Dexamethasone

•  Steroid potency

•  1× – cortisone, hydrocortisone

•  5× – prednisone, prednisolone, methylprednisolone

•  30× – dexamethasone

  Neurogenic shock – loss of sympathetic tone; usually associated with spine or head injury

•  Usually have ↓ HR, ↓ BP, warm skin

•  Tx: give volume 1st, then phenylephrine after resuscitation

  Hemorrhagic shock – initial alteration is ↑ diastolic pressure

  Cardiac tamponade (causes cardiogenic shock)

•  Mechanism of hypotension is decreased ventricular filling due to fluid in the pericardial sac around the heart

•  Beck’s triad – hypotension, jugular venous distention, and muffled heart sounds

•  Echocardiogram shows impaired diastolic filling of right atrium initially (1st sign of cardiac tamponade)

•  Pericardiocentesis blood does not form clot

•  Tx: fluid resuscitation to temporize situation; need pericardial window or pericardiocentesis

  Early sepsis triad – hyperventilation, confusion, hypotension

•  Early gram-negative sepsis – ↓ insulin, ↑ glucose (impaired utilization)

•  Late gram-negative sepsis – ↑ insulin, ↑ glucose (secondary to insulin resistance)

•  Hyperglycemia – often occurs just before patient becomes clinically septic

  Neurohormonal response to hypovolemia

•  Rapid – epinephrine and norepinephrine release (adrenergic release; results in vasoconstriction and increased cardiac activity)

•  Sustained – renin (from kidney; renin-angiotensin pathway activated resulting in vasoconstriction and water resorption), ADH (from pituitary; reabsorption of water), and ACTH release (from pituitary; increases cortisol)

EMBOLI

  Fat emboli – petechia, hypoxia, and confusion (can also be similar to pulmonary embolism [PE])

•  Sudan red stain may show fat in sputum and urine

•  Most common with lower extremity (hip, femur) fractures/orthopaedic procedures

  Pulmonary emboli (PE) – chest pain and dyspnea; ↓ PO₂ and PCO₂; respiratory alkalosis; ↑ HR and ↑ RR; hypotension and shock if massive

•  Most PEs arise from iliofemoral region

•  Tx: heparin, Coumadin; consider open or percutaneous (suction catheter) embolectomy if patient is in shock despite massive pressors and inotropes

  Air emboli – place patient head down and roll to left (keeps air in RV and RA), then aspirate air out with central line or PA catheter to RA/RV

INTRA-AORTIC BALLOON PUMP (IABP)

  Inflates on T wave (diastole); deflates on P wave (systole)

  Aortic regurgitation is a contraindication to IABP

  Place tip of the catheter just distal to left subclavian (1–2 cm below the top of the arch)

  Used for cardiogenic shock (after CABG or MI) or in patients with refractory angina awaiting revascularization

  Decreases afterload (deflation during ventricular systole)

  Improves diastolic BP (inflation during ventricular diastole), which improves diastolic coronary perfusion

RECEPTORS

  Alpha-1 – vascular smooth muscle constriction; gluconeogenesis and glycogenolysis

  Alpha-2 – venous smooth muscle constriction

  Beta-1 – myocardial contraction and rate

  Beta-2 – relaxes bronchial smooth muscle, relaxes vascular smooth muscle; increases insulin, glucagon, and renin

  Dopamine receptors – relax renal and splanchnic smooth muscle

CARDIOVASCULAR DRUGS

  Dopamine (2–5 µg/kg/min initially)

•  2–5 µg/kg/min – dopamine receptors (renal)

•  6–10 µg/kg/min – beta-adrenergic (heart contractility)

•  >10 µg/kg/min – alpha-adrenergic (vasoconstriction and ↑ BP)

  Dobutamine (3 µg/kg/min initially)

•  Beta-1 (↑ contractility mostly, tachycardia with higher doses)

  Milrinone

•  Phosphodiesterase inhibitor (↑ cAMP)

•  Results in ↑ Ca flux and ↑ myocardial contractility

•  Also causes vascular smooth muscle relaxation and pulmonary vasodilation

  Phenylephrine (10 µg/min initially)

•  Alpha-1, vasoconstriction

  Norepinephrine (5 µg/min initially)

•  Low dose – beta-1 (↑ contractility)

•  High dose – alpha-1 and alpha-2

•  Potent splanchnic vasoconstrictor

  Epinephrine (1–2 µg/min initially)

•  Low dose – beta-1 and beta-2 (↑ contractility and vasodilation)

•  Can ↓ BP at low doses

•  High dose – alpha-1 and alpha-2 (vasoconstriction)

•  ↑ Cardiac ectopic pacer activity and myocardial O₂ demand

  Isoproterenol (1–2 µg/min initially)

•  Beta-1 and beta-2, ↑ HR and contractility, vasodilates

•  Side effects: extremely arrhythmogenic; ↑ heart metabolic demand (rarely used); may actually ↓ BP

  Vasopressin

•  V-1 receptors – vasoconstriction of vascular smooth muscle

•  V-2 receptors (intrarenal) – water reabsorption at collecting ducts

•  V-2 receptors (extrarenal) – mediate release of factor VIII and von Willebrand factor (vWF)

  Nipride – arterial vasodilator

•  Cyanide toxicity at doses > 3 µg/kg/min for 72 hours; can check thiocyanate levels and signs of metabolic acidosis

•  Tx for cyanide toxicity – amyl nitrite, then sodium nitrite

  Nitroglycerin – predominately venodilation with ↓ myocardial wall tension from ↓ preload; moderate coronary vasodilator

  Hydralazine – α-blocker; lowers BP

PULMONARY SYSTEM

  Compliance – (change in volume)/(change in pressure)

•  High compliance means lungs easy to ventilate

•  Pulmonary compliance is decreased in patients with ARDS, fibrotic lung diseases, reperfusion injury, pulmonary edema, atelectasis

  Aging – ↓ FEV₁ and vital capacity, ↑ functional residual capacity (FRC)

  V/Q ratio (ventilation/perfusion ratio) – highest in upper lobes, lowest in lower lobes

  Ventilator

•  ↑ PEEP to improve oxygenation (alveoli recruitment) → improves FRC

•  ↑ Rate or volume to ↓ CO₂

•  Normal weaning parameters – negative inspiratory force (NIF) > 20, FIO₂ ≤ 40%, PEEP 5 (physiologic), pressure support 5, RR < 24/min, HR < 120 beats/min, PO₂ > 60 mm Hg, PCO₂ < 50 mm Hg, pH 7.35–7.45, saturations > 93%, off pressors, follows commands, can protect airway

•  Pressure support – decreases the work of breathing (inspiratory pressure is held constant until minimum volume is achieved)

•  Keep FIO₂ ≤ 60% – prevents O₂ radical toxicity

•  Barotrauma – high risk if plateaus > 30 and peaks > 50 → need to decrease TV; consider pressure control ventilation

•  PEEP – improves FRC and compliance by keeping alveoli open → best way to improve oxygenation

•  Excessive PEEP complications – ↓ RA filling, ↓ CO, ↓ renal blood flow, ↓ urine output, and ↑ pulmonary vascular resistance

•  High-frequency ventilation – used a lot in kids; tracheoesophageal fistula, bronchopleural fistula

  Pulmonary function measurements

•  Total lung capacity (TLC) – lung volume after maximal inspiration

•  TLC = FVC + RV

•  Forced vital capacity (FVC) – maximal exhalation after maximal inhalation

•  Residual volume (RV) – lung volume after maximal expiration (20% TLC)

•  Tidal volume (TV) – volume of air with normal inspiration and expiration

•  Functional residual capacity (FRC) – lung volume after normal exhalation

•  FRC = ERV + RV

•  Surgery (atelectasis), sepsis (ARDS), and trauma (contusion, atelectasis, ARDS) – all ↓ FRC

•  Expiratory reserve volume (ERV) – volume of air that can be forcefully expired after normal expiration

•  Inspiratory capacity – maximum air breathed in from FRC

•  FEV₁ – forced expiratory volume in 1 second (after maximal inhalation)

•  Minute ventilation = TV × RR

•  Restrictive lung disease – ↓ TLC, ↓ RV, and ↓ FVC

•  FEV₁ can be normal or ↑

•  Obstructive lung disease – ↑ TLC, ↑ RV, and ↓ FEV₁

•  FVC can be normal or ↓

  Dead space – normally to the level of the bronchiole (150 mL)

•  Area of lung that is ventilated but not perfused

•  Dead space increases with drop in cardiac output, PE, pulmonary HTN, ARDS, and excessive PEEP; can lead to high CO₂ buildup (hypercapnia)

  COPD – ↑ work of breathing due to prolonged expiratory phase

  ARDS – mediated primarily by PMNs; get ↑ proteinaceous material, ↑ A-a gradient, ↑ pulmonary shunt

•  Most common cause is pneumonia; other causes – sepsis, multi-trauma, severe burns, pancreatitis, aspiration, DIC

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