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Flashcards in Medi Deck (415):
1

Serum Na+ <135 mEq/L

Hyponatremia

  • Common Electrolyte Imbalance
  • Severe when <120 mEq/L
    • High mortality

2

Serum Osmolality

= 2Na + Serum Glucose/18 + BUN/2.8

3

ADH

Partly controls serum osmolality, released from signals in hypothalamus in response to an increase in osmolality

4

What does a serum osmolality <280 mOsm/kg indicate?

Excess total body water relative to body solutes

5

Hypertonic Hyponatremia

  • Serum Na <135 mEq/L
  • Plasma Osmolality >295 mOsm/kg
  • Causes
    • Hyperglycemia
    • Glucose Infusion
    • Mannitol Infusion (Used in Cerebral Edema)
    • Malstose Infusion (Used in IVIG Admin)

6

Isotonic Hyponatremia

  • Serum Sodium <135 mEq/L
  • Plasma Osmolality 280-295 mOsm/kg
  • Causes
    • Pseudohyponatremia (Lab Error)
      • Hyperlipidemia or Hyperproteinemia
      • Glycine in TURP, Uterine Procedures

7

Hypotonic Hyponatremia

  • Serum Sodium <135 mEq/L
  • Plasma Osmolality <280 mOsm/kg
  • Most Common
  • Further Subdivided
    • Hypovolemic
    • Euvolemic
    • Hypervolemic

8

Hypovolemic Hypotonic Hyponatremia

  • Hypovolemic (Decrease in TBW and TB Na)
    • Urine Na < or = 20 mEq/L
      • Extra-Renal Loss
        • GI Losses (Vomiting/Diarrhea/Blood Loss)
    • Urine Na > 20 mEq/L
      • Renal Loss
        • Diuretics
        • Adrenal Insufficiency
          • Low Aldosterone

9

Euvolemic Hypotonic Hyponatremia

  • Euvolemic (Increase in TBW)
    • Urine Na Always > 20 mEq/L
      • SIADH
      • Psychogenic Polydipsia
      • Potassium Depletion (Diuretic Use)

10

Hypervolemic Hypotonic Hyponatremia

  • Hypervolemic (Increase in TBW and TB Na)
    • Urine Sodium < or = 20 mEq/L
      • Edema - CHF, Cirrhosis, Nephrotic Syndrome
    • Urine Sodium > 20 mEq/L
      • Acute or Chronic Renal Failure

11

SIADH Hyponatremia

  • Excess ADH
  • Inability to dilute urine
  • Normal - High Urine Osm
  • Common cause of hyponatremia
  • Euvolemic Hypotonic Hyponatremia
  • Reduced Uric Acid
  • Normal Renal, Hepatic, and Cardiac Function
  • Causes
    • CNS Disorders
      • Meningitis, SAH
    • Pulmonary Disease
      • Pneumonia, TB
    • Cancer
      • Small Cell Lung Cancer
    • Drugs
      • Thiazide Diuretics, Chlorpropamide, SSRIs
    • Mod/Sever Hypothyroidism
      • Must R/O Thyroid disease in all pts. w/ hyponatremia

12

Psychogenic Polydipsia

  • Serum Na <135 mEq/L
  • Serum Osmolality <280 mOsm/kg
  • Urine Na always >20 mEq/L
  • Excessive water intake
  • Dilute Urine
  • Urine Osm <100 mOsm/kg

13

Exercise-Associated Hyponatremia

  • Marathons and Endurance Events
  • Increase in ADH and Excessive Water Intake
  • Urine Osm <100 mOsm/kg
  • Treatment
    • Water Restriction
    • May need hypertonic saline

14

Hyponatremia Diagnostic Work-Up

  • Labs
    • Urine Osmolality
      • >100 mOsm/kg indicates impaired ability of kidneys to dilute the urine
    • Serum Osmolality
    • Urinary Na
    • Other Labs
      • TSH/FT4
      • Uric Acid
        • Low in SIADH
      • Cortisol to R/O Adrenal Insufficiency
      • Lipids
  • Imaging
    • Head CT or CXR
      • Can assess an underlying etiology in select patients w/ suspected SIADH and cerebral salt wasting

15

Treatment Guidelines

  • Treat Underlying Disease
  • Acute vs. Chronic
    • Acute <24 hours
    • Subacute >24-48 hours
    • Chronic >48 hours
  • Mild-Moderate vs. Severe
    • Mild 130-135 mEq/L
    • Moderate 121-129 mEq/L
    • Severe <120 mEq/L
  • Asymptomatic vs. Symptomatic
  • Fluid Replacement Options
    • Normal Saline
    • Lactated Ringers
    • Hypertonic Saline (Reserved for Severe Hyponatremia)
  • Dependent on Symptoms
    • Acute
      • Severe Symptoms:
        • 100 mL of 3% NaCl IV/10 minutes x 3

16

Goals of Therapy for Acute Hyponatremia

  • Acute - Can be corrected more rapidly
    • Raise Na by 4-6 mmol/L/24hrs (Normally Less Time)
      • Not to exceed 8 mEq in 24 hours
    • Measure Serum Na Frequently

17

Goals of Therapy for Chronic Treatment

  • Minimum Correction of Serum Na 4-8 mmol/L/day
    • 4-6 mmol/L/day if risk of ODS is high
  • Correction should be SLOW
    • Rapid correction can lead to ODS

18

Osmotic Demyelination Syndrome Presentation

  • Paresis
  • Dysphagia
  • Dysarthria
  • Diplopia
  • Loss of Consciousness
  • Ataxia
  • Parkinsonism

19

Treatment of Hyponatremia

  • Hypovolemic
    • Admin isotonic/hypertonic saline
  • Euvolemic, Asymptomatic
    • Free water restriction <1L/day
      • SIADH
  • Hypervolemic
    • Treat w/ Na and fluid restriction
    • If CHF add Loop Diuretics and ACE/ARB
    • Vasopressin Antagonists
    • Correction of Underlying Condition
  • Severe Overtly Symptomatic Hyponatremia
    • Consideration of 3% saline use should be made

20

Furosemide

  • Loop Diuretic
  • Acts on ascending loop of Henle
  • Inhibits Na/K/Cl transport
  • Increases free water excretion
  • Monitor K levels

21

Desmopressin

  • Synthetic Analogue of ADH
  • Increases cAMP in renal tubular cells increasing water permeability
    • Decreases urine volume
    • Increases urine osmolality
  • Avoid in psychogenic polydipsia
  • Avoid in CHF and Cirrhosis

22

Serum Na > 145 mEq/L

Hypernatremia

23

What does water loss do to neuronal cells?

Cause them to shrink causing brain injury

24

Signs/Symptoms of Hypernatremia

  1. Lethargy
  2. Confusion
  3. Seizures
  4. Dehydration
  5. Weakness
  6. Weight Loss

25

Hypovolemic Hypernatremia

  • Loss of Na and Greater Loss of Water
    • Non-Renal
      • Urine Na < 20 mEq/L
        • GI Losses
        • Skin Losses
    • Renal
      • Urine Na > 20 mEq/L (Usually <10)
        • Loop Diuretics
        • Osmotic Diuretics

26

Euvolemic Hypernatremia

  • Loss of Water
    • Diabetes Insipidus
    • Hypodipsia

27

Hypervolemic Hypernatremia

  • Na Retention
    • Iatrogenic (hypertonic saline)
    • Mineralocorticoid Excess
      • Conn's syndrome (Primary Aldosteronism)
      • Cushings syndrome (High Cortisol)
    • Salt Ingestion

28

Diagnosis of Diabetes Insipidus

  • Labs
    • 24-Hour Urine Volume
    • Serum Electrolytes and Glucose Level
    • Urinary Na
    • Simultaneous Plasma and Urinary Osmolality 
    • Plasma ADH Level

29

Central Neurogenic Diabetes Insipidus

  • Decreased secretion of ADH
  • Causes
    • Pituitary Tumor
    • Autoimmune
    • Trauma
    • Surgery
    • Ischemic Encephalopathy
    • Idiopathic
  • Diagnosis
    • History/Physical
      • Polyuria
      • Polydipsia
      • Nocturia
    • Hypernatremia
    • High Urine Volume

30

Nephrogenic Diabetes Insipidus

  • Decreased responsiveness of ADH
  • Causes
    • Hereditary
    • Secondary to Hypercalcemia, Hypokalemia, Lithium, Demeclocycline (ADH Antagonist)

31

Primary Polydipsia (Psychogenic Polydipsia)

  • Drink large amounts of water each day
  • Does NOT result in hypernatremia
  • Polyuria
  • Water deprivation will result in rise of urine osmolalities

32

What is used to differentiate central and nephrogenic DI and primary polydipsia?

Water Deprivation Test

  • Fluid Restrict Pt
  • Follow Serum Osmolality to Steady State
    • Should approach 295 mOsm/kg
  • Administer Endogenous ADH
    • Vasopressin 5 Units SQ
    • Intranasal ddAVP 10 ug
  • Measure Serume Osmolality 1 Hour after ADH Admin

33

How should an acute case of symptomatic hypernatremia?

Should be corrected rapidly

  • Correct serum Na+
    • Initial rate of 2-3 mEq/L/h (for 2-3 hours)
      • Max Total 12 mEq/L/d
  • Measure serum and urine electrolytes every 1-2 hours
  • Perform serial neurological examinations
    • Decrease rate of correction w/ improvement of symptoms

34

How should a chronic case of hypernatremia be treated?

  • Should be corrected more slowly due to risk of brain edema
  • With no/mild symptoms should be corrected at a rate not to exceed 0.5 mEq/L/h (Total of 8-10 mEq/d)
  • If volume deficit and hypernatremia
    • Isotonic Sodium Chloride (Normal Saline)

35

What should happen after treatment of hypernatremia?

Should treat the underlying cause

36

Treatment of Central Diabetes Insipidus

  • Desmopressin (DDAVP)
    • Increases cAMP in renal tubular cells which increases water permeability resulting in decreased urine volume and increased urine osmolality

37

Treatment of Nephrogenic Diabetes Insipidus

  • Diuretics
    • Thiazides
  • Amiloride
  • NSAIDs
    • Decrease polyuria
    • Urinary retention
    • Not first line
  • Stop any medications that may cause nephrogenic DI (such as lithium)

38

Trans-tubular Potassium Gradient (TTKG)

= (KU x Osmserum) / (Osmurine x Kserum)

 

  • Assess renal potassium secretion by the cortical collecting ducts
  • Can be used to indirectly assess mineralocorticoid activity in hypo- and hyper-kalemic
  • May help determine etiology of their electrolyte imbalance

39

Serum K+ >5.5 mmol/L

Hyperkalemia

40

Causes of Pseudo-hyperkalemia

  • Excess muscle activity during venipuncture
  • Increase in cellular elements - thrombocytosis, leukocytosis, erythrocytosis
    • Causes in vitro efflux of potassium often due to hemolysis
  • Acute Anxienty During Venipuncture
  • Cooling of Blood After Venipuncture
  • Increased Uptake at High Temps may produce opposite effect
  • Genetic/Hereditary

41

Causes of Hyperkalemia

  • Pseudohyperkalemia
  • Intra- to Extracellular Shifting of Potassium
  • Inadequate Excretion
    • Meds (ACE, ARBs, K+ sparing diuretics)
  • Hyporeninemic Hypoaldosteronism
  • Renal Resistance to Mineralocorticoids
  • Advanced Renal Insufficiency
  • Primary Adrenal Insufficiency

42

EKG w/ Serum K+ of 6 mmol/L

  • Peaked T Waves
  • Flattened P Waves
  • Increased PR Interval

43

EKG w/ Serum K+ of 7 mmol/L

  • Widened QRS

44

EKG w/ Serum K+ of >10 mmol/L

  • Idioventricular Rhythm
  • Sine wave formation
  • VF ...arrest

45

EKG w/ Serum K+ of 9 mmol/L

  • Deep S Waves
  • Merging S and T Waves

46

Treatment of Hyperkalemia

  • Avoid meds that lead to K retaining
    • ACEI
    • ARBs
    • Spironolactone
    • K and Mg Supps
  • Avoid High K Foods
  • Protect heart from cardiac toxicity of hyperkalemia
    • Calcium Chloride 4ml infused over 2-3 minutes
    • Calcium Gluconate 10ml of 10% solution infused over 2-3 min
    • Patient should be on cardiac monitor during
  • Reduce plasma level of K
    • 10 Units of IV Regular Insulin immediately followed by 50 ml of 50% Dextrose Solution
    • Use of Beta Agonist (Albuterol) along w/ Insulin and Glucose 
      • Dose is 10-20 mg Albuterol in 4cc of normal saline nebulized over 10 min
    • IV Bicarb only if hyperkalemia and metabolic acidosis
  • Removal of Potassium
    • Cation Exchange Resins
      • Sodium Polystyrene Sulfonate
    • Diuretics
      • Thiazides
      • Loops
      • Should only be used in euvolemic or hypervolemic patients w/ adequate renal function
    • Hemodialysis
    • Peritoneal Dialysis (Less Effective)

47

Serum K+ <3.5 mmol/L

Hypokalemia

48

Causes of Hypokalemia

  • Pseudo-hypokalemia
  • Decreased Intake
  • Redistribution Into Cells
  • Increased Loss
    • Non-Renal
      • Diarrhea 
      • Sweating
    • Renal
      • Increased Distal Flow and Distal Na Delivery
      • Increased Secretion of Potassium
        • Mineralocorticoid Excess
      • Apparent Mineralocorticoid Excess
      • Distal Delivery of Non-Reabsorbed Anions
        • Vomiting
        • Glue Sniffing
        • PCNs
        • Mg Deficiency

49

Hypokalemic EKG Presentations

  • ST Depression
  • QT Prolongation
  • Development of U Waves
  • Vtach
  • Torsades de Pointes
    • Severe Hypokalemia (<2.5 mmol/L) plus hypomagnasemia
  • V Fib
  • PVCs

50

Treatment of Hypokalemia

  • Oral Replacement Mainstay TherapyReplace Mg first or at same time in hypomagnesemic patients to correct low K
    • Takes 100 mEq of KCl to raise serum K 1 mmol
  • Consider meds and comorbid conditions when replacing K
  • IV Replacement of Potassium
    • When Oral Route Non-Usable
    • Central Line if <2.5 mmol/L
  • Prevent Losses

51

Calcium

  • Most abundant electrolyte in body
  • 99% in Bone
  • Ionized Calcium is Biologically Active
  • Predominately Extracellular

52

Role of Calcium

  • Neuromusculary System
    • Facilitates Nerve Conduction
    • Muscle Contraction
    • Muscle Relaxation
  • Bone Mineralization
  • Cofactor for Hormonal Secretion in Endocrine Organs
  • Regulator of Ion Transport and Membrane Integrity

53

Intestinal Handling of Calcium

  • Increased Absorption
    • Puberty
    • Pregnancy Lactation
    • Vitamin D Excess
    • Acromegaly
  • Decreased Absorption
    • High Vegetable and High Fat Diet
    • Steroids
    • Senescence
    • Gastrectomy
    • Malabsorption
    • Diabetes
    • Renal Failure

54

Skeletal Handling of Calcium

  • Constantly exchanges Calcium w/ surroundings

55

Renal Handling of Calcium

  • Readily reabsorbed proximally
  • Modulation occurs in distal nephron
  • Many complex factors
    • PTH
    • Acidosis - hypercalciuria
    • Alkalosis - hypocalciuria
  • Diuretics
    • Loop - hypercalciuria
    • Mannitol - hypercalciuria
    • Thiazides - hypocalciuria
    • Amiloride - hypocalciuria

56

Hypercalcemia

  • False
    • Increase total Ca resulting from increase total proteins
  • True
    • Increase in free plasma Ca
    • Clinically relevant
  • If not known have to order an Ionized Ca level

57

Clinical Manifestations of Hypercalcemia

  • GI
    • Nausea
    • Vomiting
    • Constipation
    • Ileus
    • Pancreatitis
  • Cardio
    • Hypovolemia
    • Hypotension
    • Shortened QT
  • Renal
    • Polyuria
    • Nephrocalcinosis
  • Neuro
    • Confusion
    • Depressed Consciousness
    • Coma

58

Defense Against Hypercalcemia

  1. Increased Plasma Ca
  2. Activation of Ca sensing receptor
    1. Increases Fractional Renal Ca Excretion
  3. Decreases PTH and Increases Calcitonin
    1. Increases Fractional Renal Ca Excretion
    2. Decreases Mobilization of Ca from skeleton and soft tissues
    3. Decreases Renal 25-hydroxyvitamin D3 1a-hydroxylase
      1. Decreases calcitriol synthesis
        1. Decreases Mobilization of Ca from Skeleton and S Tissues
        2. Decreases Active Intestinal Ca Absorption

59

Treatment of Hypercalcemia

  • Saline Infusion
  • Loop Diuretics
  • Dialysis
  • Calcitonin
  • Steroids
  • IV Biphosphonates (Treatment of Choice in Cancer)

60

Causes of Hypocalcemia

  • Chronic/Acute Renal Failure
  • Vitamin D Deficiency
  • Magnesium Deficiency
  • Acute Pancreatitis
  • Hypoparathyroidism and Pseudohypoparathyroidism
  • Infusion of phosphate, citrate, or calcium-free albumin

61

Clinical Manifestation of Hypocalcemia

  • Neuromuscular Excitability
  • Hypotension
  • Decreased Cardiac Output
  • Ventricular Ectopic Activity

62

Defense Against Hypocalcemia

  1. Decreased Plasma Ca
  2. Activation of Ca sensing receptor
    1. Decreases Fractional Renal Ca Excretion
  3. Increases PTH and Increases Calcitonin
    1. Decreases Fractional Renal Ca Excretion
    2. Increases Mobilization of Ca from skeleton and soft tissues
    3. Increases Renal 25-hydroxyvitamin D3 1a-hydroxylase
      1. Increases calcitriol synthesis
        1. Increases Mobilization of Ca from Skeleton and S Tissues
        2. Increases Active Intestinal Ca Absorption

63

Treatment of Hypocalcemia

  • Oral
    • Outpatient
    • 1-3 g/d
  • IV
    • Admitted Pts.
    • Only indicated for symptomatic hypocalcemia or ionized Ca levels below 0.65 mmol/L

64

Most Common Cause of Hyperphosphatemia

Reduced Renal Phosphate Excretion (Renal Failure)

65

Clinical Manifestations Hyperphosphatemia

  • Formation of insoluble calcium-phosphate complexes
    • Soft tissues
    • Joints
    • Kidneys
  • Acute Hypocalcemia
    • Seizures
    • Tetany

66

Treatment of Hyperphosphatemia

  • Oral Phosphate Binders
    • Aluminum Salts (Up to 3g/d)
    • Calcium Salts (Up to 8g/d)
    • Non-Calcium Binders
      • Renegal
      • Fosrenal
    • Magnesium Salts (Up to 2-3g/d)

67

Hypophosphatemia

  • Moderate - 1.0 - 2.5 mg/dl
  • Severe - <1.0 mg/dl

68

Causes of Hypophosphatemia

  • Inadequate Intake (Most Common)
    • Long term Low Intake
  • Increased Excretion
    • PTH
    • Genetic Factors
  • Shift to intracellular

69

Clinical Manifestations of Hypophosphatemia

  • Metabolic Encephalopathy
  • RBC Dysfunction (May Cause Hemolysis)
  • Leukocyte Dysfunction
  • Thrombocytopenia
  • Decreased Muscle Strength and Myocardial Contractility
  • Clues to Hypophosphatemia
    • Poor Nutrition
    • Symptoms of Malabsorption
    • Exessive Antacid Use
    • Bone Pain or Fractures
    • Symptoms Suggestive of Multiple Myeloma or Other Paraproteinemia
    • Treatment w/ Parenteral Nutrition
    • Exposure to Heavy Metals
    • Use of Drugs - Glucocorticoids, Cisplatin, or Pamidronate
    • Treatment of Diabetic Ketocacidosis
    • Extensive Burns
    • Use of Growth Factors
    • Bone Marrow Transplant
    • ICU Setting
    • Treatment of HIV

70

Defense Against Hypophasphatemia

  1. Decrease Plasma Phosphate
    1. Increases tubular 25-hydoxyvitamin D3 1a-hydoxylase
      1. Increases Calcitriol
        1. Increases fractional phosphate absorption
        2. Decreases plasma PTH
          1. Increases fractional tubular phosphate reabsorption

71

Treatment of Hypophosphatemia

  • Oral Phosphate Salts (Neutraphos or IV Phosphorus)
    • Severe (<1.0mg/dl) 0.08-0.16 mmol/kg IV over 2-6 hours
    • Moderate (1.0-2.5 mg/dl) On Ventilator - 0.08-0.16 mmol/kg IV over 2-6 hours
    • Moderate (1.0-2.5 mg/dl) NOT On Ventilator - Oral 1000mg/day
    • Mild - 1000mg/day

72

Magnesium

  • Second most abundant intracellular cation in body
  • Essential cofactor for ATPase Enzymes
  • Cofactor for More Than 300 Enzyme Reactions That Involve ATP
  • Role
    • Regulates movement of calcium into smooth muscle
    • Energy transfer, storage, and use
    • Protein, Carbohydrate, and Fat Metabolism
    • Maintenance of Normal Cell Membrane Function
    • Regulation of PTH Secretion

73

What is the preferred magnesium measurement?

Serum Magnesium

  • Use is evaluating total body stores is limited
    • ECF 2% of total body magnesium
    • Doesn't always reflect ICF volume

74

Causes of Hypermagnesemia

  • Renal Insufficiency (Most Common Cause)
    • Impaired renal magnesium excretion (Cr clearance falls below 30 ml/min)
    • No a common issue
  • Hemolysis
    • Concentration in erythrocytes - 3x greater than serum
    • Will rise by 0.1 mEq/L for every 250mL of erythrocytes
    • Expected only w/ massive hemolysis

75

Clinical Manifestations of Hypermagnesemia

  • Due to Calcium Antagonism
    • Cardiac Conduction Delays
    • Depressed Contractility
    • Vasodilation

76

Treatment of Hypermagnesemia

  • Hemodialysis -treatment of choice
  • IV Calcium Gluconate (1g IV Over 2-3 Min)
  • Fluids + Furosemide

77

Hypomagnesemia

  • Common in hospitalized patients
    • 20% of pts in medical ward
    • 65% of pts in ICU
  • Typical Reference Ranges
    • Serum Mg Total - 1.4-2.0 mEq/L
    • Serum Mg Ionized - 0.8-1.1 mEq/L

78

Causes of Magnesium Deficiency

  • Diuretic Therapy (Leading Cause)
    • Most pronounced w/ loops
    • Thiazides - Only in Elderly 
    • NOT Associated w/ K Sparing
  • Antiobiotics
    • Aminoglycosides, Amphotericine, and Pentamidine
    • Blocks Magnesium Reabsorption
  • Other Drugs
    • Digitalis - shifts Mg into cells
    • Epinephrine - shifts Mg into cells
    • Cisplatin - promotes renal excretion
    • Cyclosporine - promotes renal excretion
  • Alcoholism
  • Secretory Diarrhea
  • Diabetes Mellitus
  • Acute MI

79

Clinical Manifestations of Magnesium Deficiency

  • Electrolyte Abnormalities
    • Hypokalemia - 40%
    • Hypophosphatemia - 30%
    • Hyponatremia - 27%
    • Hypocalcemia - 22%
  • Cardiac
    • Ischemia
    • Arrhythmias
    • Digitalis Toxicity
  • Hyperactive CNS Syndrome
    • Altered Mental Status
    • Generalized Seizures
    • Tremors
    • Hyperreflexia

80

Treatment of Asymptomatic Magnesium Deficiency

  • Oral Replacement
    • Sustained Release - recommended
    • Bioavailability - 33% in absence of intestinal malabsorption
      • Mag-Ox
      • Slow-Mag - Magnesium chloride
      • Mag-Tab - Magnesium lactate
    • Severe Depletion 6-8 Tablets in Divided Doses
    • Mild Depletion 2-4 Tablets

81

Treatment of Symptomatic Magnesium Deficiency

  • IV
    • 50 mEq of Mg
    • Slowly over 8-24 Hours
    • Repeat as necessary to maintain

82

CT Coronary Calcium Scoring

Never Ordered Anymore/Not Useful

Risk Stratification Only

83

CT Coronary "Virtual" Angiography

  • Can't intervene
  • Requires contrast
  • Can't fix anything and still have to put patient at risk of contrast nephropathy

84

Measurement of CAC in Asymptomatic Adult w/ 10-20% 10-year Risk?

Reasonable

85

Nuclear Scintigraphy

  • SPECT
    • Tc99 / Sestamibi (Perfusion)
  • PET
    • 18F-deoxyglucose (Metabolism)
    • 13N-Ammonia (Perfusion)
  • Great for Stress Tests
    • Sestamibi the standard
  • Can Show Myocardial Viability
  • BUT NOT Universally Available

86

Multi-Gated Acquisition Scan (MUGA)

  • IV Tracer, Stays in Blood Stream
  • Useful for Identifying Ejection Fraction
  • Still used in oncology to monitor cardiotoxicity

87

Cardiac MRI

  • Shows Muscle
    • Can show viability w/ gadolinium
  • Show Valves
  • Shows Pericardium
  • Great for Congenital Heart Disease
  • Not Widely Available
  • NOT recommended for cardiovascular risk assessment in asymptomatic adults

88

Echocardiography

  • TTE Cheap, Quick, and Available Everywhere
  • TEE Requires Sedation
    • Valve Leaflet Evaluation 
  • Great for Valve Assessment
    • Pressure Gradients
    • Doppler Flow
  • Can't Determine Viability
  • Can't See Coronaries

89

Stress Methods

  • Exercise
    • Bruce Protocol
  • Vasodilators
    • Lexiscan (Limited when BMI >50)
    • Adenosine
    • Dipyridamole
  • Inotropes
    • Dobutamine

90

Imaging Methods in Order of Increasing Sensitivity and Specificity 

  • EKG
  • Echo
  • MUGA
  • SPECT

91

Paroxysmal A Fib

  • Terminates spontaneously or w/ intervention w/in 7 days

92

Signs/Symptoms of A Fib

  • Asymptomatic
  • Palipitations
    • Skipped Heart Beats
    • Rapid Pounding in Chest
  • Fatigue
  • Chest Pain
  • Shortness of Breath
  • Stroke
  • Distal Embolization

93

A Fib Work-up

  • Hx and Physical
    • Hx of palpitations, tachycardia, fatigue, weakness, dizziness, lightheadedness
    • Symptoms of dyspnea at rest, angina, presyncope, or infrequently syncope
    • Embolic Events
    • R Heart Failure
  • Electrocardiogram
  • Echocardiogram
  • Additional Testing
    • Ambulatory Monitoring
      • Holter and Implantable Loop Monitors
      • Used when arrhythmia is intermittent
      • Cryptogenic Stroke
    • Exercise Stress Test
      • Pts w/ s/s of ischemic heart disease
      • Guide Management
    • Labs
      • Thyroid Function (TSH and Free T4) - 5% of cases w/ A Fib

94

Causes of A Fib

P.I.R.A.T.E.S

  • P - Pulmonary (PE, COPD, OSA, pneumonia)
  • I - Ischemic, Idiopathic, Iatrogenic
  • R - Rheumatic Valvular Disease, Mitral Regurg
  • A - Alcohol, Anemia, Age
  • T - Thyroid, Toxins (Stimulants, Caffeine, etc.)
  • E - Elevated BP, Electrocution, Electrolytes, Endocarditis
  • S - Sepsis, Sick Sinus Syndrome

95

Treatment of A Fib

  • New Onset
    • Symptoms usually from rapid ventricular rate
    • Rate Control
    • Identification of Embolic Risk
      • CHADS2VASc
      • TTE/TEE
    • Management of Rhythm
  • Prevention of Systemic Embolization
    • Coumadin, Dabigatran, Rivoroxaban, Apixaban
    • Valvular vs. Non-valvular
  • Rate vs. Rhythm Control
  • Hospitalization
    • Management of Heart Failure or Hypotension
    • Initiate Antiarrhythmic Drugs
    • Treatment of Associated Medical Conditions
      • Infections
      • Thyroid Storm
      • AECOPD
      • Pulmonary Embolism
      • Stroke

96

Pros and Cons of Warfarin

  • Pros
    • Old and Cheap
    • Well Studied
    • Reversible w/ Vit. K
  • Cons
    • INR Checks
    • Diet Dependent

97

Pros and Cons of NOACs/DOACs

  • Pros
    • No INR
    • Shown to be non-inferior in stroke prevention
    • Reduced risk of intracranial bleed
  • Cons
    • Eliquis/Xarelto not reversible
    • Cost
    • Not indicated in patients w/ valvular disease
    • Eliquis/Pradaxa are BID

98

Arterial Catheterization

  • Evaluate Arterial and LV Pressures
  • Evaluate LV, Aortic Valve, Mitral Valve
  • Evaluate Coronary Arteries

99

Venous Catheterization

  • Evaluate Venous and Right Heart Pressure
  • Evaluate Cardiac Output (thermodilution)
  • Evaluate Possible Shunts

100

Indications for Cardiac Catheterization

  • Symptoms of Myocardial Dysfunction
  • Symptoms of Myocardial Ischemia
  • Evaluation and Treatment of Cardiac Electrical Disease

101

Contraindications of Cardiac Catheterization

  • Absolute - NONE
  • Relative
    • Uncontrolled Ventricular Irritability
    • Uncorrected Hypokalemia or Digitalis Toxicity
    • Uncorrected Hypertension
    • Intercurrent Febrile Illness
    • Decompensated Heart Failure
    • Anticoagulated State: PT > 18 secs and INR >2.0
    • Severe Allergy to Contrast Agent
    • Severe Renal Insufficiency and/or Anuria

102

Complications of Cardiac Catheterization

  • Mortality 1:1000 to 1:100
  • 1% Treatable arrhythmias, hematomas, hemorrhage, or allergic urticaria to anaphylaxis
  • Patients w/ Increased Mortality Risk
    • Infants (<1 month) and Elderly (>85 years)
    • NYHA Class IV 10x > Class I-II
    • L Main CAD 10x> 1-2 Vessel CAD
    • Severe Aortic Stenosis w/ CAD
    • LV EF <30% 10x > EF>50%
    • Renal Insufficiency, Diabetes, Advanced Cerebrovascular Disease, Peripheral Vascular Disease, Severe Pulmonary Disease

103

Stable Angina

  • "Effort Angina"
  • Discomfort is precipitated by activity
  • Minimal or no symptoms at rest
  • Symptoms disappear after rest/cessation of activity

104

Unstable Angina

  • Crescendor or Preinfarction Angina
  • Acute Coronary Syndrome Spectrum
  • May Occur at Rest or Progressively Less Exertion
  • Severe and of Acute Onset or Longer Duration
  • Crescendo Pain - pain increases over time
  • Nocturnal Episodes

105

Microvascular Angina

  • Syndrome X
  • Angiographically normal epicardial arteries
  • "Small Vessel Disease" w/ high resistance
  • Diabetics, Women more than Men
  • Unstable Angina, Objective Evidence of Ischemia (ST-T Deviation), Elevated Biomarkers, Echo Wall Motion Abnormalities During Pain
  • Decreased Coronary Flow Reserve

106

Prinzmetal's Angina

  • AKA Variant Angina w/ Normal Coronary Vessels or Minimal Atherosclerosis
  • ST Segment Elevation (Injury Pattern) During Pain
  • May have transient Q waves
  • Angiographic hallmark is coronary spasm w/ ST elevation during chest pain
  • Provocative Testing

107

Drugs for Treatment of Acute Angina Attacks

Organic Nitrates

108

Drugs for Prophylaxis of Angina

  • Organic Nitrates
  • Beta Blockers
  • Calcium Channel Blockers
  • Ranolazine
  • K+ Channel Opener - Nicorandil

109

Organic Nitrates

  • Prodrugs that release NO →
  • Increases levels of intracellular cGMP →
  • Dephosphorylation of myosin light chain and decreased cytosolic calcium →
  • Relaxation of Smooth Muscle
  • BP my fall slightly
  • HR may increase slightly
  • CO slightly reduced

110

What is the reduction in myocardial O2 consumption by organic nitrates caused by?

  • Peripheral pooling of blood
  • Arteriolar dilation
  • Decrease in end diastolic volume and LV filling pressure

111

How can myocardial O2 consumption be determined?

  • Double Product
    • HR x Systolic BP - Approximate Measure
  • Triple Product
    • Aortic Pressure x HR x Ejection Time - Roughly Proportional

112

Progression of Drug Therapies for Angina

  • Aspirin Therapy is Always the Foundation
  • Beta Blockers Usually 2nd due to cardio-protective effects
  • Long Acting Nitrates
  • Calcium Channel Blockers
  • Late Sodium Channel Blocker
  • Statins

113

Is more than one episode of angina per week considered to be stable?

No

114

Optimal Medical Therapy for Angina Will Result In?

Less than 1 episode per week requiring more than normal levels of activity to trigger the episode

115

How to Best Treat Angina?

  • Ask more about "chest pain" as symptom
  • Examine and Document Visits Carefully
  • Watch for Changes (S4, Paradoxical Splitting of S2, Lung Congestion, Change in Quality of Pulse)
  • Quantify Functional Status (Don't Forget Erectile Dysfunction
  • DO NOT accept "I Feel OK"

116

Unstable Angina

  • Angina @ Rest
  • New Onset Exertional Angina (<2 Months)
  • Recent Acceleration of Angina (<2 Months)
  • Post Revascularization Angina

117

Pathophysiology of Acute Coronary Syndrome

  • Plaque Rupture and Subsequent Formation of Thrombus - Occlusive or Non-Occlusive
    • STEMI, NSTEMI, USA
  • Vasospasm Prinzmetals/Cocaine Use
    • STEMI, NSTEMI, USA
  • Progression of Obstructive Coronary Atherosclerotic Disease
    • USA
  • In-Stent Thrombosis
    • Early Post PCI
  • In-Stent Restenosis
    • Late Post PCI
  • Graft Dysfunction
    • Early and Late Post CABG
  • Secondary Causes
    • Thyrotoxicosis, Anemia, Tachycardia, Hypotension, Hypoxemia, Arterial Inflammation (Infection, Arteritis)

118

Aspirin and Treatment of ACS

  • Antiplatelet agent that initiates the irreversible acetylation of cyclooxygenase, thereby preventing platelet production of thromboxane A2 and decreasing platelet aggregation
  • Reduces adverse cardiac endpoints

119

ACC/AHA Guidelines for Aspirin Therapy

  • 75-325 mg/day to all patients w/ Acute Coronary Syndrome
    • Unless there is a contraindication, Clopidogrel or Prasugrel can be administered as monotherapy instead

120

Nitrates and Treatment of ACS

  • Cornerstone of anti-anginal therapy despite little objective evidence for its benefit
  • Benefit is thought to occur via reduction in myocardial O2 demand secondary to venodilation induced reduction in preload as well as coronary vasodilation and afterload reduction
  • Titrate to relife of chest pain
  • NO documented mortality benifit

121

Beta Blockers and Treatment of ACS

  • Beta blockers reduce myocardial oxygen deman by reducing heart rate, contractility, and ventricular wall tension
  • Reduces cardiac endpoints 
  • Important core measure after MI and for Acute Coronary Syndromes

122

AHA/ACC Guidelines of Beta Blocker Therapy

  • I.V. Beta blockers should be used initially in all patients w/ ACS or MI followed by oral beta blockers w/ goal being decrease in heart rate to 60 bpm
  • Combo of beta blockers and nitrates = First-Line Therapy in all patients w/ ACS

123

First-Line Therapy for ACS

Beta Blockers and Nitrates

124

Heparin and Treatment of ACS

  • Traditionally been the mainstay of therapy in ACS's as its efficacy has been documented in several large, randomized trials
  • Overall, UFH therapy generally results in an important clinical benefit
  • More effective when given in continuos infusion

125

LMWH and Treatment of ACS

  • Recent studies indicate it is also effective in reduction of end points such as MI or Death
  • When used in combination w/ ASA may be superior to continuous infusion of Heparin

126

ACC/AHA Guidline of Heparin Therapy

  • All patients w/ ACS should be treated w/ combo of ASA (325 mg/day) and heparin (bolus followed by continuous infusion w/ goal of PTT 1-2.5X control) or ASA and LMWH
  • If early PCI is planned, Bivalrudin may be used in Cath Lab rather than starting heparin in ER

127

ACE-I and Treatment of ACS

  • Reduce ventricular remodeling over days to weeks after myocardial damage
  • Data that a mortality benefit exists when used early in course of ACS
  • Reduces Cardiac Endpoints
  • May be due to improvement in endothelial function and NO release

128

AHA/ACC Guidelines fo ACE-I Therapy

  • ACE-I should be administered to all patients in the first 24 hours of ACS provided hypotension and other clear cut contraindications are absent
  • Should be initiated prior to discharge in STEMI patients w/ or w/o overt congestive heart failure

129

Statins and Treatment of ACS

  • May benefit in ACS
  • Possible mechanisms include plage stabilization, reversal of endothelial dysfunction, decreased thrombogenicity, and reduction of inflammation
  • High intensity statin therapy is initiated at the time of admission w/ ACS along w/ ASA, LMWH, Beta blocker and nitrate therapy
  • NO AHA/ACC class I indication for use in ACS

130

GPIIB/IIIA Inhibitors and Treatment of ACS

  • More potent inhibition of platelet aggregation may be of importance in patients w/ ACS that is associated w/ unstable coronary lesion and thrombus formation
  • Reduces cardiac endpoints 
  • IIB/IIIA is final common pathway for platelet aggregation

131

AHA/ACC Guidelines for Use of IIB/IIIA Inhibitors

  • Can be administered to patients whom percutaneous intervention is planned (in addition to ASA/P2Y12 Inhibitor)
  • Eptifibatide or Tirofiban can be administered to patients w/ ACS in whom PCI is not planned if other high risk feature present (TIMI Risk Score >3)

132

TIMI Risk Score

  • Predicts Risk of 14 Day MI/Death/Need for Urgent Revascularization for Patient w/ ACS
  • Scoring
    • Age >65 Years
    • Daily ASA Therapy (>7 days prior to event)
    • Symptoms of Unstable Angina
    • Documented CAD (Stenosis >50%)
    • 3 or More Traditional Cardiac Risk Factors
    • Elevated Cardiac Enzymes
    • ST Segment Deviation > .5mm
  • Scores
    • Less than 3 = Lowest risk 3-8%
    • 3 = 5-13%
    • 4 = 7-20%
    • 5 = 12-28%
    • 6-7 = 19-41%

133

Heart Score

  • Designed to separte patients needing urgent care admission from those for whome outpatient management is appropriate
  • Validated against TIMI and GRACE Scores
  • Scoring
    • History
      • Highly Suspicious = 2 Points
      • Moderately Suspicous = 1 Point
      • Slightly or Non-Suspicious = 0 Points
    • ECG
      • Significant ST-Depression = 2 Points
      • Nonspecific Repolarization = 1 Point
      • Normal = 0 Points
    • Age
      • >65 Years = 2 Points
      • >45 - <65 Years = 1 Point
      • <45 Years = 0 Points
    • Risk Factors (DM, Current or Recent
    • > or = 3 Risk Factors or History of CAD = 2 Points
    • 1 or 2 Risk Factors = 1 Point
    • No Risk Factors = 0 Points
  • Troponin
    • >3 x Normal Limit = 2 Points
    • >1 - <3 x Normal Limit = 1 Point
    • < or = Normal Limit = 0 Points
  • Scores
    • 0-3 = 2.5% MACE over next 6 weeks → Discharge Home
    • 4-6 = 20.3% MACE over next 6 weeks → Admit for Clinical Observation
    • 7-10 = 72.7% MACE over next 6 weeks → Early Invasive Strategies
  • 134

    P2Y12 Inhibitors Clopidogrel/Prasugrel and Treatment of ACS

    • Potent antiplatelet agents
    • Can be used as monotherapy all patients who cannot take ASA but usually used as dual antiplatelet therapy w/ ASA
    • Clopidogrel = 300 mg loading dose (600 mg if pre-PCI) followed by 75 mg/day
    • Prasugrel = 60 mg load followed by 10 mg/day

    135

    AHA/ACC Guidelines for Clopidogrel

    • Clopidogrel should be administered to patients who cannot take ASA because of hypersensitivity or gastrointestinal intolerance
    • In hospitalized pateints in whome an early, noninterventional approach is planned, clopidogrel should be added to ASA as soon as possible on admission and administered for at least 1 month and up to 9 months
    • DO NOT use if there is any possibility patient may be candidate for CABG

    136

    Emergent Revascularization and Treatment of ACS

    • In setting of STEMI primary PCI is associated w/ better outcomes than thrombolysis
    • Emergent PCI is also indicated in the setting of a new LBBB
    • PCI is the only effective therapy for STEMI w/ cardiogenic shock unless immediate CABG is feasible

    137

    AHA/ACC Guidelines for Primary PCI

    • Primary PCI is indicated as an alternative to thrombolysis when the following criteria are met:
      • STEMI or new LBBB
      • Can undergo PCI w/ D2B time of 90 minutes of less
      • Physician doing intervention does more than 75 PCI's/yr
      • IIA recommendation in centers w/o onsite CV surgery backup if

    138

    Approach to Chest Discomfort

    • Good History and Physical (Note Time and Duration of Symptoms)
    • Careful Evaluation of ECG (Compare to Previous When Possible)
    • Check Cardiac Enzymes
    • Monitor on Telemetry
    • Oxygen

    139

    Treatment of NSTEMI/USA

    • ASA
    • NTG (Consider MSO4 if pain not relieved)
    • Beta Blocker
    • Heparin/LMWH
    • ACE-I
    • +/- Statin
    • +/- Clopidogrel (Don't give if CABG is a possibility)
    • +/- IIB/IIIA Inhibitors (Based on TIMI Risk Score)

    140

    Treatment of STEMI

    • ASA
    • NTG (Consider MSO4 if pain not relieved)
    • Beta Blocker
    • Heparin/LMWH
    • ACE-I
    • +/- Clopidogrel (based on possibility of CABG)
    • IIB/IIIa
    • +/- Statin
    • Activate the Cath Lab!!!!!

    141

    What is diagnostic of an acute, evolving, or recent myocardial infarction?

    • Typical Rise and Fall of Troponin (Evolution of MI by Biomarker) w/ atleast 1 of following:
      • Ischemic Symptoms 
      • Development of Pathologic Q Waves on ECG
      • ST Segment Elevation or Depression
      • Echo Finding of New Wall Motion Abnormality
    • Pathological findings of an acute myocardial infarction 

    142

    Irreversible damage to myocardium can begin as early as when after interruption of blood flow? 

    20-40 Minutes After Interruption

    143

    Heart muscle can be salvaged if flow is restored within what amount of time?

    6 hours after onset of coronary occlusion

    144

    Anterior Septal Wall Infarct

    • Coronary Artery
      • LAD
    • ECG
      • V1 through V6, Q waves and ST Segment Elevations
    • Clinical Implication
      • Potential for significant dynamic compromise, CHF, Pulmonary Edema, Cardiogenic Shock, Interventricular Conduction Disturbances

    145

    Lateral Wall Infarct

    • Coronary Artery
      • Left Circumflex
    • ECG
      • I, aVL, V5, Q waves and ST segment elevations
    • Clinical Implications
      • Evaluation for posterior wall involvement, some hemodynamic changes, dysrhthmias caused by SA and AV Node Dysfunction

    146

    Posterior Wall Infarct

    • Coronary Artery
      • Left Circumflex
    • ECG
      • V1 and V2, Tall Upright R Waves w/ ST segment depression, Q waes and ST Segment Elevation in V7 through V9
    • Clinical Implications
      • Evaluation for lateral wall involvement, some hemo dynamic changes, dysarhythmias caused by SA and AV Node dysfunction

    147

    Inferior Wall Infarct

    • Coronary Artery
      • Right Coronary Artery
    • ECG
      • Q Waves and ST Segment Elevation in II, III, aVF
    • Clinical Implications
      • Evaluation of Right Ventricular Wall Involvment, some hemodynamic changes, potential for significatn arrhythmias caused by SA and AV node dysfunction

    148

    Right Ventricular Wall

    • Coronary Artery
      • Right Coronary Artery
    • ECG
      • Q Waves and ST Segment Elevations in Right Precordial Chest Leads (RV1 through RV6)
    • Clinical Implications
      • Evaluation of Inferior Wall Involvment, some hemodynamic changes, potential for significatn dysrhthmias caused by SA and AV node dysfunction

    149

    Women's Symptoms of MI

    • Sudden and Severe Fatigue Out of Proportion to Level of Activity
    • Back Pain-Especially Mid Scapular
    • Arm Heaviness w/o chest pain
    • Throat or Jaw Discomfort
    • Sudden Cold Sweat w/o pain
    • Pain radiating to back of head (cervical angina)

    150

    Exam Findings of MI's

    • Breathing may be labored
      • Fine crackles, coarse crackles, or rhonchi may be present beginning at lung base but extending upwards as CHF worsens
    • Increased BP related to anxiety and decreased CO caused by systolic dysfunction
    • Apical impulse may be diffuse or dyskinetic and a palpable S4 may be present
    • On auscultation S1 may be diminished and S2 will usually be paradoxically split
    • S4 is heard in all patients w/ MI, whereas S3 is detected in only about 10% to 20% of patients
    • Transient apical systolic murmurs may be due to papillary muscle ischemia/dysfunction
    • Inferior and RV infarcts may have parasternal (RV) lift
    • Pericardial friction rub

    151

    MI ECG Evolution

    1. Hyperacute = T Waves become Tall and Narrow
    2. ST Segments Elevate, a pattern that lasts several hours to a few days if reperfusion is not accomplished
    3. Leads facing away from injured area may show ST Segment Depression
      1. Finding is known as reciprocal ST segment changes
        1. Most likely to be seen at onset of infarction, presence does not last long
    4. Development of Q Waves
      1. Represent electrically transparent scar
      2. Usually 0.04 seconds or more in width or 1/4 to 1/3 the height of the R wave
      3. Develop w/in several hours of onset of the infarction, but may no appear until 24-48 hours after in some patients
    5. Within a few days after MI elevated ST return to baseline
      1. Persistent elevation may indicate presence of ventricular aneurysm
    6. T Waves may remain inverted for several weeks
    7. Q Waves DO NOT disappear

    152

    CK-MB

    • Appears in serum in 6-12 hours, peaks b/t 12 and 28 hours, and returns to normal in about 72-96 hours
    • Samplings performed every 4-6 hours for first 24-48 hours after onset
    • CK-MB2:CK-MB1 >1 with MI

    153

    Myoglobin

    • Release from ischemic muscle occurs earliers than CK
    • Can elevate w/in 1-2 hours of acute MI and peaks w/in 3-15 hours

    154

    Troponin

    • GOLD STANDARD for Biomarkers
    • Most cardio specific
    • Troponin I levels rise in about 1-3 hours
      • Peak at 14-18 hours
      • Remain elevated for 7-10 days
    • Troponin T levels rise in 3-5 hours and remain elevated for 10-14 days

    155

    Early Managment of MI

    • History and ECG
    • ECG Examined for presence of ST segment elevations of 1 mV or greater in contiguous leads
    1. Adminster Aspirin (160-325 mg chewed)
    2. Record 12-lead ECG, Begin Cardiac Monitoring and Repeat ECG w/in 10 minutes
    3. Administer oxygen by nasal cannula
    4. Administer sublingual NTG (Unless Systolic BP is less than 90 or HR less than 50 or greater than 100)
    5. Provide Adequate Analgesia w/ Morphine Sulfate

    156

    Thrombolytic Therarpy for MI

    • Maximal benefit if given w/in the first 3 hours after onset of symptoms
    • Sig benefit still occurs if therapy is given up to 12 hours after onset of symptoms
    • Contraindications
      • Previous hemorrhagic stroke at any time; other strokes or cerebrovascular evens w/in 1 year
      • Known intracranial neoplasm
      • Active internal bleeding (does not include menses)
      • Suspected Aortic Dissection
    • Cautions/Relative Contraindications
      • Severe uncontrolled hypertension on presentation (>180/110)
      • Hx of prior cerebrovascular accident or known intracerebral disease not covered in contraindications
      • Current use of anticoags in therapeutic doses [INR] > or = 2:3; known bleeding diathesis
      • Recent Trauma (w/in 2-4 weeks) including traumatic or prolonged (>10 minutes) CPR or Major Surgery (<3 Weeks)
      • Noncompressible vascular punctures
      • Recent Internal Bleeding (w/in 2-4 weeks)
      • Streptokinase/anistreplase prior exposure (especially w/in 5 day to 2 years) or prior allergic reaction
      • Pregnancy
      • Active Peptic Ulcer
      • Hx of Chronic Severe

    157

    What is the preferred method of emergency revascularization?

    Primary Percutaneous Coronary Intervention

    • Most effective way to reestablish blood flow

    158

    Intensive and Intermediate Care Management

    • Daily aspirin continued on indefinite basis
      • P2Y12 Inhibitor Monotherapy can be used for patients who are allergic to aspirin (Clopidogrel least expensive)
    • IV Beta Blocker should be administered w/in the initial hours of the evolving infarction, followed by oral therapy provided there are no contraindications
    • P2Y12/ASA Dual Therapy mandatory for PCI Treated Patients
    • ACE-I Administered to all patients post MI in absence of significant hypotension or allergy
    • Heparin given to patients awaiting surgical revascularization, during emergency PCI, and as part of medical therapy for ACS and Evolving MI
      • LMWH may be superior especially in NSTEMI
    • High dose atorvastatin started for both lowering LDL and stabilized plaque

    159

     Vascular Complications of MI

    • Recurrent Ischemia
    • Recurrent Infarction

    160

    Structural Complications of MI

    • LV Wall Rupture-Exsanguination or Pseudoaneurysm
    • Septal Rupture-Acute VSD
    • Papillary Muscle Rupture - Acute Mitral Insufficiency

    161

    Mechanical Complications of MI

    • Acute CHF
    • Hypotension/Shock
    • Right Ventricular Infarct
    • LV Infarct Expansion
    • Aneurysm Formation
    • Chronic Diastolic LV Dysfunction
    • Chronic Systolic LV Dysfunction

    162

    Recurrent Ischemia and Infarction

    • Incidence of postinfarction angina w/o reinfarction is 20-30%
    • Reduced incidence w/ primary PTCA
    • May be due to occlusion of an initially patent vessel, reocclusion of an initially recanalized vessel, or coronary spasm

    163

    What is the single most important predictor of mortality after acute MI?

    Left Ventricular Failure

    164

    Left Ventricular Failure

    • Single most important predictor of mortality after acute MI
    • Characterized by either systolic dysfunction alone or both systolic and diastolic dysfunction
    • Increased clinical manifestations as the extent of the injury to the LV increases
    • Advanced Age and Diabetes are other predictors of development of symptomatic LV dysfunction
    • Mortality increases with severity of hemodynamic deficit
    • LV Failure = CHF
    • Characteristically develop hypoxemia due to pulmonary vascular engorgement
    • Managed most effectively first by reduction of ventricular preload and then, if possible, by lowering afterload

    165

    Treatment of Left Ventricular Failure

    • Diuretics
    • Nitroglycerin
    • Vasodilators
    • Digitalis
    • Beta-adrenoceptor Agonists
    • Other Positive Inotropic agents

    166

    Cardiogenic Shock

    • Most severe clinical expression of left ventricular failure
    • Occurs in up to 7% of patients w/ acute MI
    • Low output state characterized by elevated ventricular filling pressures, low cardiac output, systemic hypotension, and evidence of vital organ hypoperfusion
    • At autopsy, more than 2/3 of patients w/ cardiogenic shock demonstrate stenosis of 75 percent or more of the luminal diameter of all 3 major coronary vessels and loss of about 40 percent of LV mass

    167

    Management of Cardiogenic Shock

    • Diuretics
    • Nitroglycerin
    • Vasodilators
    • Digitalis
    • Beta-adrenoceptor agonists
    • Other positive inotropic agents
    • Intraaortic Balloon Counterpulsation
    • Revascularization

    168

    Interventricular Septal Rupture

    • Occurs in 0.2 percent of patients w/ acute MI
    • Clinical Feature Associated w/ Increased Risk of Rupture
      • Lack of development of collateral network
      • Advanced age
      • Hypertension
      • Anterior location of infarction
      • Thrombolysis
    • Higher 30-Day Mortality (74%) compared to those patients who do not develop this complication (7%)
    • Size of Defect Determines the magnitude of the left to right shunt, extent of hemodynamic deterioration, likelihood of survival
    • Associated w/ complete heart block, RBBB, and Atrial fibrilation in 20-30% of cases
    • Characterized by appearance of new harsh loud holosystolic murmur
      • Best heard at lower left sternal border
      • Usually accompanied by thrill
      • Can be recognized by 2D echo
      • Surgical intervention best results

    169

    Free Wall Rupture

    • Features that characterize
      • Elderly
      • HTN
      • More frequently occurs in left ventricle
      • Seldom occurs in atria
      • Usually involves the anterior or lateral walls
      • Usually associated w/ relatively large transmural infarction involving atleast 20% of the left ventricle
      • Occurs b/t 1 day and 3 weeks, but most commonly 1-4 days after infarction
      • Most often occurs in patients w/o previous infarction
    • Usually leads to hemopericardium and death from cardiac tamponade
    • Occasionally, rupture of the free wall of the ventricle occurs as first clinical manifestation w/ undetected or silent MI, and may be considered form of sudden cardiac death
    • Course of rupture can vary from catastrophic w/ acute tear leading to immediate death, to subacute w/ nausea, hypotension, and pericaridal type of discomfort

    170

    Survival of a Free Wall Rupture Depends on What?

    • Recognition of the complication
    • Hemodynamic stabilization of the patient
    • Most importantly, prompt surgical repair

    171

    Pseudoaneurysm

    • Incomplete rupture of the heart w/ organizing thrombus and hematoma together w/ pericardium that seals the rupture
    • Over time, the area can become a pseudoaneurysm that maintains communication w/ the cavity of the left ventricle
    • Can become quite large, even equaling true ventricular cavity in size and they communicate w/ the LV cavity through a narrow neck

    172

    How to diagnose a pseudoaneurysm?

    • 2D Echo
    • Contrast Angiography

    173

    Acute Mitral Regurgitation

    • Due to partial or total rupture of a papillary muscle
      • Rare but often fatal complication of transmural MI
      • With complete rupture sudden mitral regurgitation can't be tolerated
      • Rupture of portion of papillary muscle results in severe regurgitation is much more frequent and not immediately fatal
    • Patients manifest new holosystoloc murmur and develop increasingly severe heart failure
    • Murmur may become softer or disappear as arterial pressure falls
    • Recognized by 2D Echo w/ Color Flow Doppler

    174

    Right Ventricular Infarction

    • Frequently accompanies Inferior LV Infarction
      • Rarely occurs in isolated form
    • May occur in association w/ "saddle" PE
    • Right-sided filling pressure are elevated, whereas left ventricular filling pressure is normal or only slightly raised
    • Cardiac output is often markedly depressed
    • Most have ST segment elevation in lead V4R
    • 2D Echo shows abnormal wall motion of R Ventricle as well as right ventricular dilation and depressed RV ejection fraction
    • Medications routinely prescribed for LV infarction may produce profound hypotension in patients w/ RV infarction
    • Initial treatment = volume expansion

    175

    Ventricular Arrhythmias

    • Ventricular Premature Beats (PVCs)
      • Commonly seen in acute MI
      • Usually pursue conservative approach and do not routinely prescribe antiarrhythmic drugs but instead determine whether recurrent ischemia or electrolyte/metabolic disturbances are present
    • Accelerated Idioventricular Rhythm
      • Defined as a ventricular rhythm w/ rate of 60-100 bpm
      • "Slow V Tach"
      • Seen in up to 20% of patients w/ acute MI
      • Occurs frequently during first 2 days
        • Probably results from enhanced automaticity of Purkinje fibers
      • Often observed shortly after successful reperfusion
    • Ventricular Tachycardia
      • Nonsustained paroxysms of VT may be seen in up to 67%
      • Hypokalemia and hypomagnesemia may increase risk of developing VT
      • Treatment may include
        • Amiodarone
        • Magnesium
        • Beta Blockers
    • Ventricular Fibrillation
      • Entails poor prognosis w/ an in-hospital mortality rate of 40-60%
      • Treatment = Advanced Cardiac Life Support w/ prompt Defribrillation
      • Management = Amiodarone, Revascularization by PCI

    176

    Bradyarrhythmias

    • Sinus Bradycardia
      • Common occuring during early phases of acute MI
      • Particularly frequent in patients w/ inferior and posterior infarction
      • Isolated sinus bradycardia, unaccompanied by hypotension or ventricular ectopy, should be observed rather than treated initially
      • Atropine should be utilized if hypotension accompanies any degree of sinus brady

    177

    Atrioventricular and Intraventricular Block

    • First Degree AV Block
      • Occurs in less than 15% w/ acute MI admitted to CCUs
      • Generally does not require specific treatment
        • (Digitalis, Beta Blockers, Calcium Antagonists)
    • Second Degree AV Block
      • Mobitz Type I (Wenckebach)
        • Usually transient and does not persit more than 72 hours after infarction
        • Rarely progresses to complete AV block
        • Do NOT appear to affect survival
        • Caused by ischemia of the AV Node
        • Specific therapy NOT required
      • Mobitz Type II
        • Rare conduction defect after acute MI
        • Often progresses suddenly to complete AV Block
        • Treated w/ temporary external or transvenous demand pacemaker
    • Third Degree AV Block (Complete)
      • Often develops gradually, progressing from first degree or type II second degree block
      • Treat with temporary external or transvenous demand pacemaker

    178

    Supraventricular Tachyarrythmias

    • Sinus Tachycardia
      • Typically associated w/ augmented sympathetic activity (Anxiety, persistant pain, LV Failure, Hypovolemia, Epinephrine, Atropine)
      • Beta-adrenoceptor blocking agents used to treat
    • Paroxysmal Supraventricular Tachycardia
      • Requires aggressive management because of rapid ventricular rate
      • Augmentation of vagal tone (manual carotid massage)
      • Drug of choice = Adenosine 
        • Alternative - IV Verapamil, Diltiazem, Metoprolol
    • Atrial Flutter and Fibrillation
      • Flutter - usually transient
      • Fibrillation occurs in 10-20% of patients w/ acute MI
      • Increased ventricular rate and the loss of atrial contribution to LV filling result in a significant reduction in cardiac output
      • A Fib in acute MI is associated w/ increased mortality, CVA and is a negative prognostic factor

    179

    Pericardial Effusion

    • Generally detected by 2D Echo
    • More common in patients w/ anterior MI and w/ larger infarcts and when congestive heart failure is present
    • Majority DO NOT cause hemodynamic compromise
    • When tamponade occurs, it is usually due to ventricular rupture or hemorrhagic pericarditis

    180

    Pericarditis

    • When secondary to transmural MI, may produce pain as early as first day and as late as 6 weeks after MI
    • Treatment = Aspirin at doses as high as 650 mg every 4-6 hours
      • Corticosteroids should be avoided

    181

    Dressler Syndrome

    • Post MI Syndrome
      • Autoimmune response to creation of "foreign proteins"
    • Usually occurs 1-8 weeks after MI
    • Patients present w/ 
      • Malaise, Fever, Pericardial Discomfort, Leukocytosis, Elevated ESR, and a Pericardial Effusion
    • Treatment
      • NSAIDs, Colchicine

    182

    Dilated Cardiomyopathy

    • Ventricular Dilation
      • 1 in every 3 cases of heart failure
    • Impaired Ventricular Contraction
      • May of may not develop overt heart failure
      • Symptoms usually don't appear until cardiac remodeling has been ongoing for months to years
      • EF less than 40%
    • Eventual increase in cardiac mass
    • Arrhythmia
      • Atrial or Ventricular
    • Sudden Death
      • Can occur at any stage
      • EF <35% exponential increase risk of sudden death
    • Etiology
      • Most common identifiable cause is ischemic dilated cardiomyopathy (Must rule out this cause first)
      • Idiopathic in about 50% of cases
      • Valvular Heart Disease
      • Viral Heart Disease
      • Genetic Causes
        • 1/5 to 1/3 have familial forms
        • >20 different genetic abnormalities
          • Usually related to cardiac sarcomere proteins
      • Late manifestation of hypertrophic cardiomyopathy

    183

    Ischemic Cardiomyopathy

    • Most common identifiable cause in U.S.
    • Most have known coronary artery disease
      • Can be occult disease
    • Angiography
      • Required in all paitients w/ HF of uncertain etiology
    • Must differentiate from hibernating myocardium

    184

    Infectious Causes of Cardiomyopathy

    • Viral
      • Coxsackie
      • Parvo B19
      • Adenovirus
      • Echovirus
      • CMV
      • HIV
        • Drug toxicity, secondary infection, direct toxic effect
    • Chaga's Disease
      • Trypanosoma cruzii
      • L Ventrical apical aneurysms (pathognomonic)
    • Lyme's Disease
      • Conduction Abnormality
      • Self Limited and Mild
      • Pericardial Effusion

    185

    Toxic Causes of Cardiomyopathy

    • ETOH
    • Cocaine
      • Unexplained HF in Young Patients
      • Directly Toxic
      • Infectious
    • Medications
      • Anthracycline-induced (Doxorubicin most common)
      • Trastazumab
      • Pentamidine and Zidovudine
    • Trace Elements
      • Accumulation (Cobalt, Arsenic)
      • Deficiency (Selenium, Thiamine, L-Carnitine)

    186

    Alcohol and Cardiomyopathy

    • ETOH induced apoptosis
    • Direct Toxic Effect
    • Nutritional Deficiency
      • Thiamine; beri-beri heart disease
    • Related to both mean daily intake and duration of use
      • 80-90g per dary for more than five years
    • Similar in Men and Women
      • Women seem to be more sensitive to effects
    • Arrhythmias
      • Holiday Heart Syndrome
      • Atrial Fibrillation Most Common

    187

    Inherited Causes of Cardiomyopathy

    • Neuromuscular Disorders
      • Muscular Dystrophies
      • Myotonic Dystrophy
    • Hereditary Hemochromatosis (Most common disorder)
    • Hereditary Sideroblastic Anemias
    • Thalassemias

    188

    Systemic Disease and Cardiomyopathy

    • Systemic Lupus Erythematosus
    • Sarcoidosis
    • End-Stage Renal Disease
    • Celiac Disease
    • Endocrine Dysfunction
      • Thyroid, Pheochromocytoma, Cushing's Syndrome, Growth Hormone
    • Obstructive Sleep Apnea

    189

    Peripartum Cardiomyopathy

    • HF that develops during the last trimester or w/in 6 months of delivery
    • Cause usually unknown
      • Inflammatory myocarditis, immune, or gestational HTN
    • More common in multiparous women of African ancestry
    • Mortality around 10%
    • Pts who recover from heart failure should be encouraged to avoid future pregnancy

    190

    Hypertrophic Cardiomyopathy

    • Genetic Disorder
    • Hypertrophy of a wall of the L Ventricle (occasional R Ventricle)
      • Most commonly the interventricular septum
      • Concentric
      • Apical
    • Highly variable manifestations and morphologies
    • Diastolic dysfunction is usually present
    • Obstruction of L Ventricular Outflow
    • Manifestations
      • Often asymptomatic
        • Found during family screening
      • Increased outflow gradients
      • Women are usually older at presentation w/ worse symptoms
      • Sudden Cardiac Death
    • Autosomal Dominant
      • Incomplete penetrance
      • 1 in 500 in general population
    • Myocardial beta myosin heavy chain
    • Cardiac myosin-binding protein C
    • Acquired Causes
      • Hypertension
      • Aortic Stenosis

    191

    Most Common Cause of Cardiac Hypertrophy and Ventricular Dysfunction

    • Hypertension
    • Aortic Stenosis

    192

    Restrictive Cardiomyopathy

    • Nondilated Ventricles
      • Walls rigid
    • Impaired ventricular filling
      • Diastolic Dysfunction
    • Hypertrophy Absent
    • Systolic Function Normal
      • At least early
    • Less Common
    • Idiopathic
    • Infiltrative and Storage Diseases
      • Amyloidosis and Hemochromatosis
    • Endomyocardial Scarring; myocardial fibrosis and eosinophilic endocarditis (Loeffler's)

    193

    Stress Induced Cardiomyopathy

    • Transient L Ventricular Apical Ballooning
    • Precipitated by intense psychologic stress
      • Usually sudden onset
    • Postmenopausal Women
      • Normal Coronary Arteries Usually

    194

    Arrhythmogenic Right Ventricular Dysplasia

    • Ventricual wall replaced by fibrous and fatty tissue
    • Function abnormal
    • Regional akinesis or dyskinesis
    • Young patients

    195

    Left Ventricular Noncompaction

    • Rare, unclassified L Ventricular Cardiomyopathy
    • Interruption of compaction of the meshwork of the L Ventricular muscle during development

    196

    Systolic Dysfunction

    • Decreased myocardial contractility
    • Reduced L Ventricular EF
    • Initially CO is maintained
      • LV enlargement; increased stroke volume
      • Frank-Starling relationship
    • Over time CO decreases and HF symptoms begin

    197

    Diastolic Dysfunction

    • L Ventricular Filling is Abnormal
    • Elevated Filling Pressures
    • May occure w/ or w/o systolic dysfunction
    • More difficult to identify and may be missed or underestimated
    • Characterisitic of both hypertrophic and restrictive cardiomyopathy
    • L Ventricular Relaxation
      • Isovolumic Relaxation
      • Passive Filling Dependent of Compliance
      • Active Filling During Atrial Contraction

    198

    Leading cause worldwide of heart failure?

    Coronary Artery Disease

    199

    NYHA Class I

    • No limitation on physical activity
    • No overt symptoms

    200

    NYHA Class II

    • Slight limitation on physical activities
    • Comfortable at rest, but ordinary physical activity causes symptoms of heart failure

    201

    NYHA Class III

    • Marked limitation on physical activities
    • Comfortable at rest, but less than ordinary activity causes symptoms of heart failure

    202

    NYHA Class IV

    • Inability to carry on any activity w/o symptoms
    • Presence of symptoms even at rest

    203

    Pathogenesis of HFrEF

    • Myocyte hypertrophy
    • Alteration in contractile properties
    • Loss of myocytes
    • Beta adrenergic desensitization
    • Abnormal myocardial metabolism
    • Reorganized structural collagen weave
    • Important factors
      • Neurohormones, TNF, growth factors (endothelin), superoxide
    • Left Ventricular Remodeling

    204

    Symptoms of Heart Failure

    • Cardinal Symptoms
      • Dyspnea and Fatigue
      • Orthopnea
      • Paroxysmal Nocturnal Dyspnea
      • Cheye-Stokes Respiration
      • Acute Pulmonary Edema

    205

    History and Physical Exam Seen w/ Heart Failure

    • General Appearance 
      • Cachexia
    • Vital Signs
    • Jugular Veins
      • Low Sensitivity
    • Pulmonary
      • Rales
      • Expiratory Wheeze
    • Cardiac
      • Cardiomegaly, Parasternal Impulse (Heave), Abnormal Heart Tones/Murmurs
    • Abdomen
      • Ascites, Hepatomegaly
    • Extremities
      • Edema

    206

    Diagnosis of Heart Failure

    • Routine Labs (Help manage)
      • Secondary Causes, Renal Function, Electrolytes
    • ECG (Not really diagnostic)
      • LVH, QRS Width
    • Chest X-ray
      • Pulmonary edema and cardiomegaly
    • Echo (Most importan diagnostic tool)
      • LV Function and Size
    • Biomarkers
      • Helpful in diagnosis and prognosis
    • Exercise Stress Testing
      • Assess for Ischemia

    207

    Treatment of HFpEF

    • Stabilize HR and BP
    • Improve Exercise Tolerance
    • Decrease Hypertensive Heart Disease
    • ACE-I/ARBs (Must be on one of them)
    • Calcium Channel Blockers
    • Beta Blockers (Must be on one of them)
    • NO ROLE for Digitalis in HFpEF

    208

    Treatment HFrEF

    • Neurohormonal Antagonism

    209

    Other Medications for Heart Failure

    • Digoxin
      • Mild Inotropic Effects
    • Oral Diuretics
      • Salt and Water Constriction Cornerstone
    • Ca Channel Antagonism
      • BP Reduction
    • Statins
    • Anticoagulation/Antiplatelet
    • Fish Oil
    • Exercise

    210

    Other Treatments for Heart Failure

    • Cardiac Resynchronization Therapy
    • Sudden Cardiac Death Prevention
    • Surgical Treatment
      • CABG
      • Surgical Ventricular Restoration
      • Mitral Regurgitation
      • Transplant and L Ventricular Assist Devices
    • Gene and Cellular Based Therapy

    211

    Approach to Management of Acute Decompensated Heart Failure

    • Identify the Cause
    • Airway Assessment and Measurement of Oxygen Saturation
    • Ventilatory Support
    • Cardiac Monitoring
    • IV Access
    • Patient Positioning
    • Diuretic Therapy
    • Vasodilator Therapy
    • Urine Output Monitoring

    212

    Oxygen and Respiratory Support

    • Supplemental Oxygen ONLY if SpO2 <90%
    • For Respiratory Distress Consider Positive Pressure Support

    213

    Diuretic Therapy for Acute Decompensated Heart Failure

    • IV Loop Diuretic
    • Early Intervention may produce better outcomes
    • Typically these patients are volume overloaded
    • AVOID w/ Cardiogenic Shock
    • Aortic Stenosis (USE W/ CAUTION)
    • Monitor Urine Output, Vital Signs, Oxygenation, Daily Weights, Kidney Function Markers, and Electrolytes
    • May repeat doeses depending on expected response
      • Bolus Dosing or IV Drips
    • Serum K and Mg should be monitored daily
    • Lower Central Venous and Pulmonary Capillary Wedge Pressure
    • Reduction in Left and Right Heart Filling Pressures
    • Augmented Stroke Volume and Cardiac Output
    • BUN and Serum Creatinine Expected to Rise

    214

    Vasodilator Therapy for Acute Decompensated Heart Failure

    • Reduce Elevated Filling Pressure
    • Reduce Left Ventricular Afterload
    • Indicated for Patients w/ need for urgent afterload reduction
      • HBP
      • Acute Mitral Regurg
      • Acute Aortic Regurg
    • Adjunct to diuretics
    • Use w/ Caution

    215

    Nitroglycerin for Heart Failure

    • Reduce L Ventricular Filling Pressure
      • Venodilation
      • Higher doses lower systemic vascular resistance and LV Afterload
    • IV rather than transdermal or oral
    • Tachyphylaxis can occur w/in hours
      • Nitrate free intervals to avoid
    • Nitroprusside
      • Cyanide poisoning

    216

    Fluid and Sodium Constriction for Acute Decompensated Heart Failure

    • <2g/day
    • Fluid Restriction of 1.5-2.0 L/day
      • Best for refractory HF or Hyponatremia
      • Inconclusive data in trials

    217

    Important Measures

    • DVT Prophylaxis
    • Fluid Monitoring
      • Accurate In/Out
    • Daily Weights
    • Electrolytes and Renal Function

    218

    Inotropic Agents for Acute Decompensated Heart Failure

    • For Cardiogenic Shock
    • Dobutamine
      • Beta-1 Adrenergic Agonists
    • Dopamine
      • Dopamine-1 agonists at low doses
      • Beta-2 and alpha-1 agonist at high doses
    • Milrinone
      • Phosphodiesterase Inhibitor
    • Severe Refractory LV Dysfunction and Low Output
      • Severe Hypotensive w/ signs of end organ damage

    219

    Swan-Ganz Catheters

    Right Heart Catheterization

    220

    Right Heart Catheterization

    • Balloon tipped catheter is inserted into jugular or femoral vein and fed through R Atrium, R Ventricle, Pulmonary Artery and Pulmonary Capillary Wedge Position (Indirect estimate of L Atrial Pressure)
    • Measure Pressures at each location
    • Sample Blood at each location for oxygen saturation to diagnose cardiac shunts

    221

    Indications for Right Heart Catheterization

    • Differentiate b/t types of shock
    • Evaluate for pulmonary hypertension
    • Determine cause of pulmonary edema
    • Diagnose L to R Shunt
    • Diagnose Pericardial Tamponade

    222

    Complications of Right Heart Catheterizations

    • Arrhythmia (Most Common)
    • Pulmonary Artery Rupture
    • Arterial Puncture
    • Pneumothorax
    • RBBB
    • Knotting of the Catheter
    • Infection
    • Pulmonary Infarct

    223

    Cannon A Waves

    • Atrial contraction against closed tricuspid valve
      • Occurs in V. tach and Junctional rhythms

    224

    Large V Waves

    Tricuspid Regurgitation

    225

    Normal CVP

    3-8

    226

    Normal Systolic RVP

    15-30

    227

    Normal Diastolic RVP

    3-8

    228

    Normal Systolic PAP

    15-30

    229

    Normal Diastolic PAP

    4-12

    230

    Normal PCWP

    2-15

    231

    Normal Systolic LVP

    100-140

    232

    Normal Diastolic LVP

    3-12

    233

    CVP or RA Waveform

    • A Wave = Atrial Contraction
    • C = Closure of Tricuspid Valve
    • X Wave = Atrial Diastole
    • V Wave = Passive Atrial Filling
    • Y Descent = Atrial Emptying

    234

    Elevated RAP

    • Think:
      • Tricuspid Regurgitation
      • Tricuspid Stenosis
      • Volume Overload
      • Pulmonary Hypertension
      • Constrictive Pericarditis
      • Cardiac Tamponade
      • R Ventricular Infarct
      • Pulmonic Stenosis
      • L to R Shunt

    235

    Elevated CVP

    Think Biventricular Heart Failure

    236

    If RAP = RV End Diastolic Pressure = PCWP

    Consider cardiac tamponade, constrictive pericarditis, or restrictive cardiomyopathy

    237

    Elevated PAP

    • Causes
      • Left Ventricular Failure
      • Pulmonary Hypertension
      • Hypervolemia
      • Mitral Valve Disease

    238

    Causes of Elevated PCWP

    • LV Failure, Systolic or Diastolic
    • Constrictive Pericarditis
    • Mitral Stenosis
    • Mitral Insufficiency
    • Aortic Insufficiency
    • Cardiac Tamponade

    239

    PCWP Normal and PAP Elevated

    Pulmonary Arterial Hypertension

    240

    PCWP of 15-25 will result in?

    Dyspnea on Exertion

    241

    PCWP of 25-35 will result in?

    Dyspnea at Rest

    242

    Acute rise in PCWP >35 will result in?

    Pulmonary Edema

    243

    Systemic Vascular Resistance Calculation

    SVP = ((MAP - CVP) / CO) x 80

    244

    Pulmonary Vascular Resistance Calculation

    PVR = ((PAP-PAWP) / CO) x 80

    245

    How is a L to R Shunt Detected?

    By step up in oxygen saturation of blood in RA, RV, or PA compared to the mixed venous oxygen saturation

    246

    Pulmonary Hypertension

    • Elevated pressures in pulmonary arteries
    • Diagnosis requires R Heart Cath and a PA Resting Pressure > or = 25
    • Echo can be very suggestive of PH if estimated PASP is >50
    • Cause elevated R ventricular pressures, remodeling, and eventual failure
    • Progressive and if untreated fatal, disease

    247

    Symptoms of Pulmonary Hypertension

    • Initial Symptoms
      • Exertional Dyspnea
      • Lethargy
      • Fatigue
    • Later Symptoms
      • Exertional Chest Pain
      • Exertional Syncope
      • Anorexia or Abdominal Pain From Hepatic Congestion
      • Peripheral Edema
    • Ortner's Syndrome
      • Congestion, Cough, and Hoarseness
        • L Recurrent Laryngeal Nerve compressed by dilated main pulmonary artery

    248

    Pulmonary Hypertension Physical Exam Findings

    • Increased Jugular Venous Pressure
    • Decreased Carotid Pulse Pressure
    • Amplified Pulmonic Component of 2nd Heart Sound
    • R Sided 4th Heart Sound
    • Tricuspid Regurgitation
    • CXR
      • Enlarged Central Pulmonary Arteries
    • EKG
      • R Axis Deviation and R Ventricular Hypertrophy
    • Echo
      • Decreased LV size and increased RV and RA Size
      • Tricuspid Regurgitation
    • Pulmonary Function Tests (Often COPD could be cause)
    • CT of Chest (Interstitial lung disease)
    • Perfusion Scan (Pulmonary embolism could be cause)

    249

    Pulmonary Hypertension Labs

    • ANA
    • RF
    • ANCA
    • LFT's
    • HIV
    • TSH

    250

    Pulmonary Hypertension Workup

    1. Echo
      1. If not suggestive of PH find another diagnosis
      2. If suspicion very high then R Heart Cath
      3. If suggestive of PH
        1. L Sided Heart Disease?
          1. Yes
            1. Does it account for the degree of elevation in pulmonary artery pressure?
              1. Yes - no further studies
              2. No - R Heart Cath
          2. No
            1. R Hear Cath

    251

    Group 1 Pulmonary Hypertension

    • Pulmonary Arterial Hypertension
      • Idiopathic Pulmonary Arterial Hypertension
        • Sporadic
          • No cause can be determined
          • Mostly females
          • 2 per million
        • Heritable
          • 20% of IPAH
          • Autosomal dominant w/ incomplete penetrance
      • PAH due to disease affecting the small muscular pulmonary arterioles
        • Connective Tissue Diseases
        • HIV
        • Congenital Heart Disease
        • Portal Hypertension
      • PAH due to drugs and toxins
        • Definite Increased Risk
          • Anorexigens: aminorex, fenfluramine, dexfenfluramine
          • Toxic Rapeseed Oil
        • Probable Increased Risk
          • Cocaine
          • Amphetamines
          • Methampthetamines
          • SSRI's
          • Phentermine
          • L-tryptophan
          • Chemotherapy
          • St. John's Wort
          • Phenylpropanolamine
          •  

    252

    Group 2 Pulmonary Hypertension

    • Due to L Sided Heart Disease (Pulmonary Venous Hypertension)
      • L Ventricular Diastolic or Systolic Dysfunction
      • Mitral Valve Disease
      • Pulmonary Venoocclusive Disease

    253

    Group 3 Pulmonary Hypertension

    • Due to hypoxemia or lund disease
      • COPD
      • Interstitial Lung Disease
      • OSA
      • Alveolar Hypoxia
        • Neuromuscular Disease
        • Diaphragmatic Paralysis
        • Thoracovertebral Deformities

    254

    Group 4 Pulmonary Hypertension

    • Chronic thromboembolic pulmonary hypertension
      • 1-3.8% of patients following acute pulmonary embolism
      • Some patients may have a hypercoaguable state
      • Surgical thromboendarterectomy if lesion accessible

    255

    Group 5 Pulmonary Hypertension

    • W/ unclear multifactorial mechanisms
      • Myeloproliferative disorders
      • Sarcoid
      • Sickle Cell
      • Glycogen Storage Diseases
      • Beta Thalessemia

    256

    Treatment of Pulmonary Hypertension

    • Exercise
    • Diuretics
      • Decreased peripheral edema
      • Decrease R Ventricular Volume Overload
    • O2 as indicated for hypoxemia
    • Anticoagulation

    257

    Treatment of Idiopathic PAH

    • High Dose Calcium Channel Blockers
      • Only in those that respond to short acting vasodilators during cardiac cath w/ PA pressures dropping by 10% or more and final mean pressure of <40
      • Only 20% of IPAH respond to CCBs over long term
    • Endothelin Receptor Antagonists
    • Phosphodiesterase-5-Inhibitors
      • Prolong vasodilatory effect of NO
    • Prostacyclin Agonists
      • IV have greatest efficacy but high risk of infections
    • Lung Transplant
      • Consider after IV Prostacyclin has failed and patient still having R Heart Failure

    258

    Cor Pulmonale

    • Dilation or hypertrophy of the R Ventricle and subsequent impaired function due to pulmonary hypertension caused by lung disease or pulmonary vascular disease
      • Does not include R Sided HF due to L Sided Heart Disease or Congenital Heart Disease)
    • 50% of cor pulmonale is due to chronic bronchitis and COPD
    • Acute rise in pressue causes dilation and failure
    • Chronic ris in pressure can cause hypertrophy and then dilation and failure

    259

    Symptoms of Cor Pulmonale

    • Dyspnea (Most Common)
    • Edema
    • Fatigue
    • Ascites
    • Abdominal Pain
    • Exertional Syncope
    • Cough Related Syncope
    • Hepatomegaly
    • Tachypnea
    • Lethargy
    • Exertional Angina
    • Elevated JVP
    • R Ventricular Heave
    • "Carvallo's Sign"
      • Holosystolic murmur (from tricuspid regurg) louder w/ inspiration
    • Cyanosis - late finding
    • Pulmonary edema - late finding (R Ventricle bows into L Ventricle)

    260

    Diagnosis of Cor Pulmonale

    • Must r/o L Heart Failure is it is the most common cause of R Heart Failure
    • Same as Pulmonary Hypertension but w/:
      • Mean PAP > or = 25
      • Elevated RVEDP
      • Elevated CVP
      • NO L Heart Disease

    261

    Treatment of Cor Pulmonale

    • Treat underlying disease
    • Decrease work of breathing w/ non invasive ventilation and bronchodilators
    • O2 to keep SpO2 >90
    • Correct respiratory acidosis
    • Transfuse if anemic
    • Medications
      • Diuretics
      • Pulmonary vasodilators for PAH
      • Inotropes
        • Dobutamine or Milrinone for Cardiogenic Shock due to Cor Pulmonale

    262

    Goal of Peroperative Evaluation

    • Inform the surgeon, anesthesiologist, patient, and other stakeholders of estimated risk related to proposed procedure
    • Mitigate those risks, where possible
    • Anticipate adverse events, and guide management

    263

    Peroperative Evaluation

    • Assess Cardiac Risk (MACE, MI, etc.)
    • Assess pulmonary risk
    • Assess thromboembolism risk
    • Other risk (Renal, Endocrine, Psych, etc)
    • Prophylactic Antibiotics

    264

    Cardiac Risk Assessment

    • Goldman (Modified) Risk (RCR)
    • Gupta Risk Calculator
    • ACS-NSQIP Calculator
    • Functional Capacity
      • Can take care of self (1 MET)
      • Can walk up flight of steps or a hill (4 METs)
      • Can do heavy work around the house (4-10 METs)
      • Stenous Sports (>10 METs)
    • Needs to be adjusted based on patient history

    265

    Pulmonary Risk

    • Less Well Defined 
    • Sleep Apnea
      • Post-Extubation Pulmonary Edema
      • Post-op respiratory failure
    • Lifetime Tobacco Exposure
    • Current Smoking
    • Bronchiectasis
    • Asthma

    266

    Preop VTE Prophylaxis

    • Standard of Care
    • Doing nothins IS NOT ACCEPTABLE

    267

    What is the single biggest preventable risk with orthopedic surgery?

    DVT

    268

    Isolated Proteinuria can be caused by?

    1. Overproduction - Bence Jones Proteinuria
    2. Tubular Dysfunction - Fanconi's
    3. Glomerular Dysfunction

    269

    What urine test should be ordered in all diabetic patients?

    Urine Micro-albumin

    270

    Mild Isolated Proteinuria

    • <1g/day
    • Stressful Conditions
      • Fever
      • Exercise
      • CHF
    • Overproduction of Light Chains, Heavy Chains, Bence Jones, B2-Microglobin, Hemoglobinuria

    271

    Orthostatic Proteinuria

    • 1-2 g/day
    • 2-5% of Adults
      • More common in adolescents and uncommon in age >30
    • Cause may be hemodynamic, subtle glomerular change, entrapment of renal vein on left by aorta and superior mesenteric artery

    272

    Recurrent or Persistant Hematuria

    • Presence of excessive number of RBCs in urine
      • >2/HPF in centrifuged urine is pick up by dipstick
    • <10% in adults due to kidney - usually due to prostate, bladder, urethra
    • Non-Glomerular Causes of Hematuria
      • Neoplasm
      • Trauma
      • Vascular Disease
      • Hypercalcemia
      • Cysts
      • Medullary Sponge or Cystic Kidneys
      • Hydonephrosis
      • Interstitial Nephritis

    273

    Glomerular Hematuria

    • Characterized by microscopic RBCs distorted by osmotic/chemical stress as they pass through the nephron
    • Proteinuria > 2 g/day and hematuria enhance the possibility that hematuria is glomerula
    • MOST COMMON CAUSES of ASYMPTOMATIC hematuria are IgA Nephropathy and Thin Basement Membrane Nephropathy

    274

    Nephrotic Syndrome

    • > 3.5 g protein/day
      • Edema
      • Hyperlipidemia
        • Increased cholesterol due to overproduction of liver due to decrease in oncotic pressure
        • Acquired defect in LDL receptor that results in diminished clearance
        • Increased triglycerides due to decreased catabolism NOT overproduction
      • Hypoproteinemia
    • MOST COMMON CAUSES
      • Membranous Nephropathy
      • Focal Segmental Glomerulosclerosis
    • Additional Consequences
      • Hypothyroid
      • Low 1,25-hydroxyvitamin D3
      • Decreased total serum calcium
      • Decreased Immunoglobins
      • Malnutrition
      • Thromboembolic Disease - decreased anti-thrombin III levels
      • Coagulation Abnormalities

    275

    Nephritic Syndrome

    • MOST COMMON CAUSES
      • Crescenteric Glomerulonephritis
      • Endocapillary Proliferative Glomerulonephritis
      • IgA Nephropathy

    276

    ANCA - Associated Vasculities

    • Wegener's
      • Granulomatous inflammation involving respiratory tract
      • Necrotizing vasculities of small to medium vessels
      • Necrotizing GMN
    • Microscopic Polyangitis 
      • Necrotizing vasculities of small to medium vessels 
      • Necrotizing GMN
      • Pulmonary Capillaries Involved
    • Chrug-Strauss
      • Eosinophil rich and granulomatous involvement of respiratory tract
      • Necrotizing vasculities of small/medium vessels
      • Blood eosinophilia
      • Asthma
      • Ectopy
    • Epidemiology
      • 5-7th Decade
      • Male Predominance
      • White > Black
    • Clinical Presentation
      • ALL have signs of vasculities
      • Renal involvement greater in Wegener's and Polyangitis (RPGN)
      • Constitutional Symptoms
      • Cutaneous Involvment - Purpura
      • Respiratory in Wegener's and Chrug/Straus
      • Peripheral Neuropathy - Most Common in Chrug Strauss

    277

    Pathogenesis of ANCA - Associated Vasculities

    • ANCA
      • Most Common are PR3-ANCA and MPO-ANCA
        • cANCA has specificity for PR3 (Wegener's)
        • pANCA has specificity for MPO (Pauci-Immune Crescenteric GMN)

    278

    Treatment of ANCA - Associated Vasculities

    • Wegener's
    • Microscopic Polyangitis
    • Chrug-Strauss
      • Prednisone 1 mg/kg/day plus Cytoxan 2mg/kg/day
        • For induction therapy
      • Wean prednisone to 10 mg/day at 3 months
      • After 3-6 months may change Cytoxan to Azathioprine for 18-24 months

    279

    Minimal Change Disease

    • Primary Glomerular Disease
    • MOST COMMON in Children
    • 10-15% of GMN in Adults (3rd Most Common)
    • May be male preponderance 2:1 in children but disappears in adults
    • Higher propensity for elderly to develop acute renal failure
    • Pathogenesis
      • Most likely consequence of T lymphocyte abnormalities
      • T cells may produce a product that increases *glomerular permeability*
      • Loss of charge-selective barrier
      • Other mechanisms - IgM rheumatoid factor, Circulating Immune Complexes
      • Podocytopathy - causes effacement of podocytes
    • Clinical Features
      • Abrupt onset of nephrotic syndrome
        • Avg. Proteinuria 10 g/day
      • Hypertension uncommon
        • 30% in Children
        • 50% in Elderly
      • Hematuria Uncommon
      • Renal Failure Uncommon
        • More common in elderly and NSAIDs
    • Lab Findings
      • Severe Proteinuria - Rapid Onset
      • Sed Rate Increased
      • Low Albumin
      • Increased Cholesterol and Trigylcerides
      • Normal Renal Function
    • Pathology
      • No Findings on Light Microscope
      • Minimal Staining on Immunofluorescence
      • Effacement of visceral epithelial foot processes on electron microscopy
    • Treatment
      • Prednisone 1 mg/kg/day - adults (NOT to exceed 80 mg/day) or 2 mg/kg/day every other day
        • Prolonged treatment, about 16 weeks, more evident in adults
        • Treat 8 weeks then taper down dose
        • Rearrangement of actin cytoskeleton is reversible w/ glucocorticoids
      • Cyclosporin
        • 2-5 mg/kg/day for 3 months then slowly taper, continue therapy at minimal dose for 1-2 years
          • IF steroid resistant or dependent

    280

    Focal Segmental Glomerulosclerosis

    • Increasing prevalence in US
      • Accounts for 20-25% of all GMN
    • African-Americans 4-fold increase in ESRD due to genetic risk factors
    • MOST COMMON GN Leading to ESRD
    • Pathogenesis
      • Poorly understood
      • Some injurious factor
      • Podocytopathy not reversible w/ steroids
        • Detach from GBM
        • Unable to repair themselves by cell division leads to glomerulosclerosis
      • Viral Induced Disease - HIV
      • Drug Induced Disease - Interferon
      • Hemodynamic Adaptations
    • Clinical Features
      • Proteinuria of varying degree
      • Hematuria in >50%
      • Renal Failure in 33%
      • Hypertension in 33%
      • Increased degree of proteinuria 
    • Classification
      • Focal Sclerosis
      • Perihilar Variant
      • Cellular Variant
      • Tip Variant - Highest Treatment Response Rate
      • Collapsing Variant - Worse Prognosis
    • Treatment
      • Prednisone 1 mg/kg/day for 6 months
      • IF steroid resistant or dependent Cyclosporin 3-5 mg/kg/day for 4-6 months
        • May respond better if treated up to 1 year

    281

    Membranous Glomerulopathy

    • Epidemiology
      • MOST COMMON CAUSE of Nephrotic Syndrome in Adults and Elderly (25%)
      • Peak incidence is 4th - 5th decade
      • More common in middle-aged males 
      • 20-25% of cases associated w/ Malignancy and Infection
    • Pathogenesis
      • Autoimmune Glomerulonephritis
      • IgG Antibody to Podocyte Membrane Antigen
        • IgG4 antibody to PLA2R
        • IgG4 antibody to THSD7A - More common in females and malignancies
    • Clinical Features
      • 70-80% present w/ Nephrotic Syndrome
      • Hypertension in 13-55%
      • Most present w/ normal to slightly increased creatinine
      • 4-52% may develop renal vein thrombosis
      • Persistence proteinuria and renal insufficiency are poor prognostic indicators
      • Male gender, older, age, uncontrolled hypertension portend poor prognosis
      • Coexist w/ glomerular lesion
      • Most frequent lesion related w/ carcinoma
      • Spontaneous vascular thrombosis - most common
    • Lab Findings
      • Nephrotic Proteinuria - Hallmark
      • Normal Complement Levels
      • Elevated LDL and VLDL - common
      • Enhanced hypercoagulable state
    • Pathology
      • Stage I
        • Subepithelial dense deposits w/o adjacent basement membrane reaction
      • Stage II
        • Projections of basement membrane adjacent to deposits
      • Stage III
        • Deposits surrounded by basement membrane
      • Stage IV
        • Thickened basement membrane w/ irregular lucent zones
    • Treatment
      • Alternating course of steroids w/ cyclophosphamide 
        • Solu-Medrol - 1 g/day for 3 days on 1, 3, 5 months then prednisone 0.5 mg/kg/day for 27 days
        • Alternate w/ oral cyclophosphamide 2.0-2.5 mg/kg/day on months 2, 4, 6
      • Cyclosporin 
        • May be used initially or again in steroid resistant or dependent patients
        • 3-5 mg/kg/day for at least 6 months
        • If proteinuria not reduced by 50% discontinue
        • If patient has complete remission taper over 3-4 months
        • If patient has partial remission continue for 1-2 years
      • Tacrolimus 
        • 0.05-0.075 mg/kg/day w/ prednisone
      • Rituximab 
        • 375 mg/kg weekly times 4
      • Anticoag therapy if serum albumin is < 2.5 g/dl - controversial

    282

    Membranoproliferative Glomerulonephritis

    • Characterized by:
      • Persistent antigenemia and circulating immune complexes w/ glomerular deposition
      • Diffuse proliferative lesions in mesangium and capillary wall, widening of capillary loops w/ double contour
      • Older Adults (>30) frequently associated w/ cryoglobulinemia and Hepatitis C
    • Epidemiology
      • Less than 5% of all primary glomerulonephritis
      • Equal proportion of males to females
      • Decreasing in frequency
      • 5-10% of Nephrotic Syndrome
      • More common in caucasians
    • Pathogenesis
      • Type I
        • Probably immune complex disease
        • Inflammation caused by immune complexes causes proliferation of mesangium and endothelial cells
        • Hepatitis C
      • Type II
        • Deposits of dense material (Dense Deposit Ds) w/in basement membrane, Bowman's capsule, and tubules
        • Deposits activate C3
      • Hypocomplementemia is characteristic feature in ALL types
    • Clinical Features
      • Usually that of Nephrotic Syndrome
      • 25-33% present w/ acute Nephritic Syndrome
      • Hypertension is mild
      • 50% have renal dysfunction
      • Type II have poorer prognosis, Very Rare
    • Lab Findings
      • Hematuria - Hallmark presentation
      • Another hallmark is complement abnormalities - C3/CH50 persistently depressed
      • C3 Nephritic Factor enhances complement activation - Found in Dense Deposit Disease
        • Autoantibody that reacts w/ convertase of C3
    • Treatment
      • Type I - Treat Underlying Disease
        • Cytoxan or MMF plus Prednisone for 6 Months - For patient w/ Nephrotic Syndrome and declining renal function
      • Type II - Good Therapy Lacking

    283

    Rapidly Progressive Glomerulonephritis

    • Clinical Features
      • Rapid loss of renal function
      • Oliguria or Anuria
      • Proteinuria
      • Dysmorphic Erythrocyturia
      • Extensive crescent formation
      • Three Major Immunopathologic Categories
        • Immune Complex Glomerulonephritis
        • Pauci-Immune Glomerulonephritis
        • Anti-Glomerular Basement Membrane Glomerulonephritis
    • Treatment
      • SoluMedrol IV 1 g daily for 3 days
      • Prednisone and Cytoxan following

    284

    IgA Nephropathy (Berger's Disease)

    • Epidemiology
      • MOST COMMON Glomerulonephritis in the World
      • Predominent IgA Deposition in Mesangium
      • Clinical features span asymptomatic hematuria to gross hematuria to crescenteric glomerulonephritis
      • Most Common in 2nd and 3rd Decade of LIfe
      • Much more common in males
      • Synpharyngitic Macroscopic Hematuria is classic clinical syndrome
      • 10-15% of patients <40
      • Gross Hematuria at Time of Acute Pharyngitis
    • Pathogenesis
      • Circulating Glomerular Immune Complexes of Galactose-Deficient IgA1 (IgG Autoantibody)
        • Inheritable Trait (Major dominant gene)
        • Environmental triggers may lead to increased production of IgA1
      • Deposition of IgA1 in mesangium
    • Treatment
      • ACE and ARB agents combined for mild disease w/o proteinuria
      • Steroids for 6 months taper over 12 w/ addition of Azathioprine if no response (if 1-3 g of protein)
      • Tonsillectomy - Controversial
      • Fish Oil - if proteinuria > 1g/day
      • Cytotoxic agents for progressive disease
      • Long term treatment w/ ACE or ARB agent and titrate dose to proteinuria <1 g/day
      • Patients w/ persistant proteinuria >1 g/day despite 3-6 months of therapy w/ ACE or ARB treat w/ 6 months of steroids STOP ACE or ARB. ADD Fish Oil

    285

    Goodpasture's

    • Autoimmunity to a specific component of the GBM
    • Associated w/:
      • Crescenteric GMN (Linear IgA deposits)
      • Alveolar Hemorrhage
      • Circulating anti-GBM antibodies
      • Other clinical symptoms
      • Antibodies typically IgG
    • Clinical Features
      • Peak incidence 3rd and 6th decade
      • Male predominance; Caucasian
      • Most present w/ RPGN and Lung Hemorrhage
      • 30-40% only renal involvement
      • 30% may have positive p-ANCA
    • Predisposing Factors
      • Genetic Predisposition - HLA DR2
      • Infectious Agents - Influenza
      • Smoking - Hydrocarbons
      • Urinary Infection, Lithotripsy, or Pre-Existing GMN
    • Lab Features
      • Almost all have circulating anti-GBM antibodies
      • In correct clinical setting positive test can be used as indication to start treatment w/o biopsy, but Biopsy Preferred
      • Widespread Crescents
      • Lesions are Monophasic
    • Treatment
      • Combined therapy w/ plasma exchange, steroids, cyclophosphamide

    286

    Diabetic Nephropathy

    • Hallmarks of Disease
      • Hypertension
      • Progressive Increase in Proteinuria
      • Progressive Decline in GFR
    • GFR remains stable in Type 2 until hypertension and persistent proteinuria develops
    • Rate of decline w/ established nephropath is 5-10 ml/min/year
      • Correlates w/ systolic blood pressure

    287

    Who should be screened w/ microalbuminuria?

    • Type I diagnosed for more than 3-5 years and over 12 years should be screened yearly
    • All Type 2 Diabetics yearly screening
    • Those w/ elevated UAER every 6 months

    288

    Risk Factors fo Progression of Microalbuminuria

    • Glycemic Control
    • Genetic Predisposition 
    • Male
    • Age at Diagnosis 
    • Mean Arterial BP >95mmHg
    • Smoking
    • Hyperlipidemia
    • Retinopathy

    289

    Conditions Associated w/ Increased Albumin Excretion

    • Retinopathy
    • Peripheral Neuropathy
    • Hyperglycemia
    • Obesity
    • Atherogenic Lipid Profile
    • Coronary Heart Disease
    • LVH

    290

    Diabetic Treatment Regimens

    • SGLT-2 Inhibitors (If GFR good use this)
      • Have been showm to lower HbA1c, lead to weight loss, and lower BP
      • Lower GFR and Reduce Albuminuria
      • Empagliflozin (Jardiance)
    • DPP-4 Inhibitors (For lower GFRs)
      • Lower albuminuria and lower GFRs
      • Linagliptin (Tradjenta)
      • Sitagliptin (Januvia)

    291

    Antihypertensive Therapy

    1. ACE/ARB
    2. Salt Restriction and Diuretic Use
    3. Diltiazem or Verapamil
    4. Carvedilol or Nebivolol
    5. Aldosterone Inhibition
      1. Difficult to use because of hyperkalemia

    292

    What statin can increase proteinuria and decrease renal function?

    Rosuvastatin

    293

    If GFR <30, what should daily protein intake be decreased to?

    0.8 g/kg/day

    294

    Stages of Chronic Kidney Disease

    • Stage 1 - Damage w/ Normal GFR
      • >90 ml/min
    • Stage 2 - Damage w/ Mild Decrease GFR
      • 60-89 ml/min
    • Stage 3 - Modere Decrease GFR
      • 30-59 ml/min
    • Stage 4 - Severe Decrease GFR
      • 15-29 ml/min
    • Stage 5 - Kidney Failure
      • <15 ml/min no dialysis
    • Stage 6 - End Stage Kidney Disease
      • <15 ml/min on dialysis

    295

    Uremia

    Advanced stage of CKD when multiorgan system dreangements become clinically manifest

    296

    MOST useful test for diagnosis of Uremic Coagulopathy?

    Bleeding Time

    297

    Shock

    State in which profound and widespread reduction of effective tissue perfusion leads to reversible and, if prolonged, irreversible cellular injury

    298

    Circulatory Shock

    Syndrome in which tissue perfusion is reduced such that blood flow is inadequate to meet cellular metabolic requirements

    299

    Hypovolemic Shock

    • Decreased effective circulating volume
    • CO = Decreased
    • SVR = Increased
    • PAOP = Decreased
    • Causes
      • Hemorrhagic
        • Trauma
        • GI
        • Retroperioneal
      • Increased Vascular Capacitance (Vasodilation)
        • Sepsis
        • Anaphylaxis
        • Toxin/Drugs
      • Fluid Depletion (Nonhemorrhagic)
        • External Fluid Loss
          • Dehydration
          • Vomiting
          • Diarrhea
          • Polyuria
        • Interstitial Fluid Redistribution
          • Thermal Injury
          • Trauma
          • Anaphylaxis
    • Degree of Volume Loss and Response
      • 10% Loss - well tolerated (tachycardia)
      • 20-25% Loss - failure of compensatory mechanisms (hypotension, orthostasis, decreased CO)
      • >40% Loss - overt shock (marked hypotension, decreased CO, lactic acidemia)

    300

    Obstructive Shock

    • Impaired cardiac filling, low cardiac output
    • CO = Decreased
    • SVR = Increased
    • PAOP = Increased or Normal
    • Causes
      • Impaired Diastolic Filling (Decreased Preload)
        • Direct Venous Obstruction
        • Intrathoracic Obstructive Tumors
        • Pregnancy
        • Intra-abdominal Hypertension
      • Increased Intra-Thoracic Pressure
        • Tension Pneumothorax
        • Mechanical Ventilation (w/ excessive pressure or volume depletion)
        • Asthma/COPD
        • Decreased Cardiac Compliance
        • Constrictive Pericarditis
        • Cardiac Tamponade
      • Impaired Systolic Contraction (Increased Ventricular Afterload)
        • R Ventricle
          • Pulmonary Embolus (Massive)
          • Acute Pulmonary Hypertension
        • L Ventricle
          • Aortic Dissection

    301

    Cardiogenic Shock

    • Cardiac failure (pumping)
    • CO = Decreased
    • SVR = Increased 
    • PAOP = Increased
    • Causes
      • Myopathic
        • MI (hibernating myocardium)
        • L Venticle
        • R Ventricle
      • Myocardial Contusion
      • Septic Myocardial Depression
      • Cardiac Tamponade
      • Arrhythmic
        • Bradycardia
        • Tachycardia (e.g. atrial fibrillation)
      • Pharmacologic
        • Anthracycline Cardiotoxicity
        • Calcium Channel Blockers
        • Beta Blockers

    302

    Distributive Shock

    • Inappropriate peripheral vasodilation
    • CO = Increased
    • SVR = Decreased
    • PAOP = Normal
    • Causes
      • Septic
        • Can cause myocardial depression
      • TSS
      • Anaphylactic, Anaphylactoid
      • Neurogenic (Spinal Shock)
      • Toxic (e.g., Drug Overdose)

    303

    Sepsis

    • Systemic response that is caused by the presence of pathogenic microorganisms and/or their toxins (super-antigens) in the bloodstream
    • Pathogenesis
      • Life-threatening organ dysfunction caused by dysregulated host response to infection and/or superantigen
      • Know the main microbial triggers
        • Gram Negative = Endotoxin (LPS)
        • Gram Positive = Exotoxins, Superantigens, Enterotoxins, Lipoteichoic Acid Peptidoglycans, Hemolysins
      • Know Pro-Inflammatory Cytokines
        • IL 1, 6, and 12
        • TNF-alpha
        • IFN-gamma
      • Can lead to
        • Endothelial cell damage causing leakage out of vessels
        • Thrombosis leading to poor perfusion of organs and organ failure
        • Depletion of clotting factors leading to more leakage from the vasculature

    304

    Early Sepsis

    • aPc levels decrease early in sepsis due to consumption
      • Activates Protein C
      • Inhibits Va, VIIIa
    • Rapidly produces hyper-coagulable state
      • aPC requires endothelial thrombomodulin to be activated

    305

    Sepsis-3 Sepsis Definition and Clinical Criteria

    • Life threatening organ dysfunction caused by dysregulated host response to infection
    • Suspected or Documented infection + acute increase of 2 or greater SOFA points

    306

    Quick Sofa

    • RR > 22
    • sBP <100
    • Altered GCS

    307

    Sepsis-3 Septic Shock Definition and Clinical Criteria

    • Subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality
    • Clinical Criteria
      • Sepsis + Vasopressor therapy needed to elevate
      • MAP > or = 65 + lactate >2 despite adequate fluid resuscitation

    308

    Most Frequent Sites of Infection in Sepsis Patients

    • Lungs
    • Abdomen
    • Urinary Tract

    309

    Community Acquired Pneumonia

    Strep pneumoniae

    310

    Hospital Acquired Pneumonia

    Gram negative aerobes (E. coli, Klebsiella, etc)

    311

    Toxic Shock Syndrome

    Staph. aureus

    312

    Leading cause of neonatal sepsis

    Strep agalactiae

    313

    Common Causes of Neonatal Sepsis

    • Strep. agalactiae
    • E. coli

    314

    Common Causes of Sepsis in Children

    • Strep. pneumoniae
    • Neisseria meningitidis
    • Staph aureus

    315

    What affects patient outcomes of sepsis?

    • Predisposition
      • Host dependent, gender difference?
      • TNF polymorphism (TNF-beta2 showed increased mortality)
      • TLR 4 Asp299Gly allele found exclusively in patients w/ septic shock
    • Recognition
      • PCR
      • Procalcitonin, CRP
      • Endotoxin assay
      • Pneumonia diagnostics
    • Response
      • Pro-inflammatory vs. Anti-inflammatory
      • Immunomodulation
        • GCSF Administration
        • aPC/Antithrombin - FAIL
        • Corticosteroids
        • IV Polyclonal Immunoglobulin Administration

    316

    Prevention of Organ Failure

    • Early Recognition
    • Early Treatment
    • Early Resuscitation
    • Optimize Glucose Control
    • Optimize Hemodynamics
    • Organ Protection

    317

    Surving Sepsis Campaign Protocol

    • To be completed w/in 3 hours of time of presentation
      • Measure lactate level'
      • Obtain blood cultures prior to admin of antibiotics
      • Administer broad spectrum antibiotics
      • Administer 30 ml/kg crystalloid for hypotension or lactate > or = 4 mmol/L
    • To be completed w/in 6 hours
      • Apply vasopressors to maintain MAP > or = 65
      • In event of persistent hypotension after initial fluid admin, re-assess volume status and tissue perfusion and document findings
      • Re-measure lactate if initial lactate elevated
    • Reassessment of Volume Status and Tissue Perfusion
      • Either
        • Repeat focused exam by licensed independent practitioner including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings
      • Or TWO of the Following
        • Measure CVP
        • Measure ScvO2
        • Bedside cardiovascular ultrasound
        • Dynamic assessment of fluid responsiveness w/ passive leg raise or fluid challenge

    318

    Choice of Antimicrobial Agent - Factors to Consider

    • Host Factors
      • Concomitant disease status or use of immunosuppressive medications
      • Prior adverse drug effects
      • Impaired elimination or detoxification of the drug
      • Age of the patient
      • Pregnancy status
      • Epidemiologic Exposure
    • Pharmacologic Factors
      • Kinetics of absorption, distribution, and elimination
      • Ability of the drug to be delivered to the site of infection
      • Potential toxicity of an agent
      • Pharmacokinetic or pharmacodynamic interactions w/ other drugs

    319

    Physiologic Compensation to Shock

    • Small decreases in fluid volume are easily tolerated
    • Large decreases in blood volume elicit range of compensatory responses in an effort to restore the ECBV
      • Mechanisms will eventually fail, if patient not supported
    • Response to Low ECBV
      • About 10% Decrease
        • No change in arterial pressure or cardiac output
      • About 20% Decrease
        • CO begins to fail, but pressure is maintained
      • > 20% Decrease
        • Arterial pressure begins to fall
    • Mechanisms
      • Baroreceptor Reflex
      • Chemoreceptors
      • Cerebral Ischemia
      • Endogenous Vasoconstrictors
      • Reabsorption of tissue fluids
      • Renal retention of Na and Water

    320

    If ECBV is not corrected in time, what happens?

    Decompensation that leads to further reduction in arterial pressure and possible death

    321

    Baroreflex

    • Elicited by fall in ECBV and will increase sympathetic output to the heart, peripheral circulation, and adrenal medulla
      • Increase HR and SV
      • Arterial Vasoconstriction
      • Venoconstriction

    322

    Chemoreceptor Reflex

    • Elicited when MAP falls below 60
    • Low pressure and low flow leads to hypoxia and acidosis
      • Stimulate peripheral chemoreceptors in carotid sinus to increase ventilation which helps to minimize the acidosis
      • Increases arterial pO2
      • Stimulation of respiration increases venous return and enhances lymphatic flow

    323

    Cerebral Ischemia

    • Elicited when MAP fall below 40
    • Perfusion of the brain will be compromised, resulting in cerebral ischemia
      • Massive sympathetic and adrenal discharge causing marked vasoconstriction and increased myocardial contractility
      • Increased parasympathetic outflow to the heart results in a decrease in heart rate and small decrease in myocardial VO2

    324

    What does vasoconstriction and low ECBV do to capillary hydrostatic pressure?

    Decreases it, thus changing Starling Forces (net hydrostatic force < net oncotic force) favoring reabsorption from interstitial space

    325

    Components of Decompensation Associated w/ Shock

    • Cardiac Failure
    • Vascular Failure
    • Metabolic Acidosis
    • Central Nervous System Depression
    • Inappropriate Clotting
    • Depression of the Mononuclear Phagocytic System

    326

    Cardiac Failure and Shock

    • Low MAP leads to low coronary perfusion and in adequate oxygen delivery resulting in coronary ischemia
    • Low cardiac output causes poor peripheral perfusion, resulting in vasodilation and further decreases arterial pressure
    • Further decreases coronary perfusion

    327

    Vascular Failure and Shock

    • Inappropriate vasodilation

    328

    Metabolic Acidosis and Shock

    • Shift in glycolytic metabolism from fall of CO and compromised tissue perfusion and oxygen delivery
      • NET EFFECT
        • Production of increasing abouts of lactate leading to lactic acidosis
        • Further depresses cardiac function

    329

    CNS Depression and Shock

    • From decreased cerebral blood flow
      • Elicits marked sympathetic outflow to try and increase arterial pressure to increase flow to the brain
      • As MAP unable to rise sufficiently, progressive cerebral hypoxia and CNS depression eventually results in failure of sympathetic output
      • Endogenous opioids are released are also depress CNS function

    330

    Clotting and Shock

    • Early on, hypercoagulabilty 
    • Later, during decompensation this devolves into hypocoagulation and fibrinolysis

    331

    Mononuclear Phagocytic System (MPS) and Shock

    • During hemorrhagic hypotension, is depressed
      • Impairs antibacterial and antitoxin defense systems
      • Endotoxins from the gut flora, which are usually inactivated by the MPS, begin to increase causing vasodilation that exacerbates the shock

    332

    Presentation of Shock

    • Hypotension
    • MAP <60
    • Tachy
    • Cool Extremities/Mottling
      • Might be warm later in stages of septic shock
    • Oliguria
    • Clouded Sensorium
    • Elevated Lactate

    333

    Approach to Patient w/ Shock

    • Rapid Assessment Balanced w/ Decisive Action
    • Recognition of Cause
    • What kind or patient are we dealing w/?
      • Trauma - head involve?
      • Unknown and Unresponsive
      • Pertinent History
      • Known Infection
      • Previous Surgery
      • Emphysemia
      • CAD
    • Physical Exam and Treatment (Need to happen simultaneously)
      • Obtain good IV access
        • 18 g and/or central line
      • Foley Catheter
      • Evaluate Level of Consciousness
        • Consider Intubation
      • SBP
      • MAP
      • Look for Respiratory Failure
      • PE: heart tones, breath sounds, mottling
      • Arterial line placement?
      • Initiate fluid resuscitation
        • AND MONITOR RESPONSE
        • If no improvement = vasopressor therapy
      • Imaging
        • CXR
        • Echo?
        • CT Scan??? (Later on when stable)
      • Labs
        • ABG
        • CBC
        • CMP
        • Coagulation Parameters
        • Cardiac Enzymes
        • Lactate
        • Blood Cultures

    334

    Goals of Therapy for Shock

    • MAP > 60
    • Improvements in clinical criteria
      • Increased Urine Output
      • Improvement in Mental Status Change
      • Etc.
    • Treatment of underlying cause

    335

    What is the first choice vasopressor?

    Norepinephrine (Levophed)

    336

    What is the second choice vasopressor?

    Epinephrine (Beware of tachycardia)

    337

    Gold Standard for Evaluation of Trauma Patient

    CT Scan (Surgically)

    338

    First Core Measure of Resuscitation of Sever Hemorrhagic Trauma Patient

    Stop Bleeding

    339

    Acute Kidney Injury

    Abrupt decline in GFR resulting in accumulation of nitrogenous waste (urea nitrogen & creatinine) & dysregulation of extracellular volume & electrolytes

     

    • Increase in SCr >0.3 mg/dl w/in 48 hours
    • Increase in SCr > 1.5 times baseline w/in prior 7 days
    • Urin Volume <0.5 ml/kg/hr for 6 hours

    340

    Stages of Acute Kidney Injury

    • Stage 1
      • 1.5-1.9 times baseline or increase creatinine > 0.3 mg% or output < .5 ml/kg/hr for 6-12 hours
    • Stage 2
      • 2.0-2.9 times baseline or output < .5 ml/kg/hr for >12 hours
    • Stage 3
      • 3.0 times baseline or creatinine > 4.0 mg% or output < .3 ml/kg/hr for 24 hrs or anuria >12 hrs

    341

    Etiology of Acute Kidney Injury

    • Acute Tubular Necrosis (45%)
    • Pre-Renal (21%)
    • Acute or Chronic Kidney Disease (13%) - due to prerenal & ATN
    • Obstruction (10%) - Mostly men w/ prostate disease
    • Glomerulonephritis and Vasculitis - RPGN (4%)
    • Acute Interstitial Nephritis (2%)
    • Atheroembolic (1%)

    342

    Risk Factors for Acute Kidney Injury

    • Age
    • Gender
    • Proteinuria
    • Diabetes 
    • CHF
    • Sepsis
    • CKD
    • Volume Depletion
    • Chronic Liver Disease
    • Hyperuricemia

    343

    Acute Kidney Injury Classification

    • Prerenal
      • Hypovolemia
      • Reduced Effective ECV
    • Renal
      • Renal Artery Occlusion
      • Renal Vein Occlusion
      • Renal Perenchymal
        • Intrarenal Vascular
        • Glomerulonephritis
        • Ischemic Acute Tubular Necrosis
        • Toxic ATN
        • Interstitial
        • Intrarenal Obstruction
    • Post Renal
      • Urinary Tract Obstruction

    344

    Causes of Prerenal Acute Kidney Injury

    • Reduced Effective ECV
      • Hypovolemia
      • Cardiac Failure
      • Systemic Vasodilation
    • Impaired Renal Autoregulation
      • Preglomerular (Afferent Arteriolar) Vasoconstriction
      • Postglomerular (Efferent Arteriolar) Vasodilation

    345

    Pathophysiology of Prerenal AKI

    • Caused by reduction in glomerular perfusion
    • Most are caused by a decrease in effective intra-arterial volume
    • Autoregulation of Renal Blood Flow
      • Remain remarkably constant despite wide variations in BP & renal perfusion pressure from 70-150
      • Promotes Afferent Arteriolar Vasodilation
      • Tubular-Glomerular Feedback
    • Autoregulation of GFR
      • Combined affarent arteriolar vasodilation and efferent arteriolar vasoconstriction
        • Increases filtration fraction
      • Angiotensin II constricts the efferent arteriole and is predominant influence

    346

    Muddy Brown Casts

    ATN

    347

    Prerenal Failure Lab Values

    • High BUN:Creatinine Ratio >20:1
    • Urine Chemistry
      • Uosm - >500
      • Urine Na+ - <10
      • Fractional Na+ Excretion - <1%

    348

    Acute Tubular Necrosis

    • Pathogenesis
      • Proximal tubule and medullary thick ascending limb of loop of henle are segments most susceptible to ischemia and nephrotoxins
    • Course
      • Initial Phase
        • Period when exposed to ischemia or toxins and parenchymal injury is evolving but not yet established
      • Maintenance Phase
        • Parenchymal injury is established and GFR stabalizes at a value of 5-10 ml/min
          • Urine output is lowest
          • Typically lasts 1-2 weeks but may be prolonged to 1-11 months
      • Recovery Phase
        • Period during which patients recover renal function through repair and regeneration of renal tissue
        • Initially there is gradual rise in urine output and decrease in creatinine
          • May develop polyuria and diuretic phase of ATN
          • Caused by diuresis from salt and water accumulation 
            • Osmotic diuresis from retained urea and other osmotic substances

    349

    Postrenal Acute Kidney Injury

    • Caused from obstruction
      • Could be cancer

    350

    Treatment of Acute Kidney Injury

    • Essentially treating underlying cause
    1. Intravascular Volume Depletion
      1. Blood - if cause is hemmorrhage
      2. Crystalloids
        1. NaCl is fluid of choice until stabilized
          1. Add K, bicarb, etc if necessary
    2. Decreased "Effective" Volume
      1. CHF - optimize cardiac output
        1. Nitrates, ACE, diuretics, inotropic agents
      2. Bacterial Sepsis - causes excessive vasodilation and intrarenal vasoconstriction
      3. Cirrhosis - Lasix and Spironolactone
    3. Impaired Renal Compensatory Responses
      1. Volume depletion kidney has ability to compensate
        1. STOP NSAIDs and ACE inhibitors
    4. Increased Intrarenal Vasoconstriction
      1. Hepatorenal Syndrome, Radiocontrast, Hypercalcemia, Cyclosporine, Sepsis, and Tacrolimus
        1. No clinical benefit for Dopamine - (increases renal diffusion at low doses) but may cause arrhythmias
        2. Avoid dehydration, monitor drug levels, limit dose of radiocontrast, and treat hypercalcemia 
    • DO NOT USE
      • Dopamine
      • Fenoldopan
      • ANP
      • Diuretics to prevent AKI
      • Acetylcysteine
    • Additional Recommendations 
      • Keep blood sugar 110-149 mg/dl
      • Avoid protein restriction to prevent dialysis
      • Nutrition 20-30 kcal/kg/d via enteral route
      • Vasopressors for BP support as necessary

    351

    Dialysis Therapy

    • Indications
      • Uremia
      • Hyperkalemia - K > 6.5 or 5.5-6.5 w/ ECG changes
      • Fluid Overload - resistant to diuretics, espicially pulmonary edema
      • Metabolic Acidosis - pH<7.2 despite sodium bicarb therapy
    • Outcomes
      • High cost of care
      • Increased mortality
      • Increased length of hospital stay
      • Development/Progression to CKD w/ need for chronic dialysis

    352

    Hepatorenal Syndrome

    • Potentially reversible functional renal failure that occurs in patient w/ acute or chronic liver disease
    • Profound renal vasoconstriction in the setting of histologically normal kidneys
      • Resembles prerenal azotemia
      • Defining feature is lack of improvement w/ volume expansion
    • Pathogenesis
      • Impaired Na and Water handling leads to fluid retention causing ascites and edema
      • Primary mechanism is decrease in splanchnic and systemic vascular resistance leads to
        • Hyperdynamic circulation
        • Activate Vasoconstrictor Systems
    • Pathophysiology
      • Reduction in SVR due to primary arterial vasodilation in the splanchnic circulation, triggered by portal HTN
      • Stage 1
        • Portal HTN is moderate and increased cardiac output compensates for the decreased vascular resistance
      • Stage 2
        • Severe portal HTN, cardiac output CANNOT compensate, vasoconstrictor systems turned on
      • Renal Consequences
        • Mechanisms help maintain effective vascular volume but cause Na/Water retention which leads to ascites and edema
          • Leads to renal failure by causing intense cortical intrarenal vasoconstriction and hypoperfusion
        • Renal failure rarely occurs in cirrhosis w/o ascites

    353

    Clinical Patterns of Hepatorenal Syndrome

    • Type I
      • Rapid decline in renal function w/ at least doubling of creatinine to > 2.5 or reduction of creatinine clearance by 50% or more to <20ml/min, over duration of <2 weeks
      • Usually seen in hospitalized pts w/ advanced cirrhosis or fulminate hepatic failure
      • Low Survival (Mean of 2 weeks)
      • >90% Mortality at 3 Months
    • Type II
      • Moderate or stable reduction in GFR (creat 2.0)
      • Insidious onset and slow progression in setting of refractory ascites
      • Better prognosis, mean survival 6 months w/o treatment

    354

    Triggering Events of Hepatorenal Syndrome

    • Hypovolemia
    • Bacterial Infection
    • GI Bleed
    • Diuretics
    • Diarrhea
    • Spontaneous Bacterial Peritonitis - COMMON
    • NSAIDs

    355

    Diagnosis of Hepatorenal Syndrome

    • Chronic or Active Liver Disease (Advanced)
    • Low GFR - creat. >1.5 or GFR <40
    • NO Shock, Fluid Loss, Infection, or Toxic Drugs
    • NO improvement w/ volume 1.5 liters or albumin IV 1g/kg to max of 100 g/d
    • NO Proteinuria <500/day
    • Urinalysis
      • Volume <500 ml/d
      • Na <10 mEq/L
      • FeNa < 1
      • Urine Osmolality > Serum Osmolality
      • Urine RBCs < 50
      • Serum Na < 130 mEq/L

    356

    Cardiorenal Syndrome

    • Disorders of heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other
    • 5 Types
      • Type 1 - Acute CHF (MAIN Type)
      • Type 2 - Chronic Cardiac Dysfunction Leads to CKD
      • Type 3 - Abrupt and Primary Worsening of Kidney function causes acute cardiac dysfunction
      • Type 4 - Primary CKD contributes to cardiac dysfunction
      • Type 5 - Acute or Chronic Systemic Disorders lead to both cardiac and renal dysfunction
    • Predictors
      • CAD
      • Diabetes
      • Hx of Prior CHF
      • High dose diuretics
      • Tachy
      • Edema
    • Pathophysiology
      • Neurohormonal Adaptations
      • Reduced Renal Perfusion
      • Increased Renal Venous Pressure - Reduces GFR
      • R Ventricular Dilatation and Dysfunction
    • Pathogenesis
      • Decreased CO w/ LOW renal perfusion
      • Activation of RASS
      • Anemia
      • Meds - NSAIDs, ACE/ARB
      • Right Ventricular Dysfunction
      • MAIN is volume overload and venous congestion leading to AKI
        • Renal Venous HTN
        • Ascites w/ increased intra-abdominal pressure
        • Secondary Inflammation

    357

    Treatment of Cardiorenal Syndrome

    1. Loop Diuretics - either bolus or infusion
    2. ACE/ARB Agents
    3. Beta-Blockers - Cautious Use
    4. Vasodilators
    5. Inotropes - Dobutamine
    6. Dialysis
    • Prognosis
      • Increased Morbidity and Mortality

    358

    Patient Presenting w/ Chest Pain Work-U[

    • Broad, high-liability differential
    • CXR
    • 12-Lead EKG
    • Cardiac Enzymes
    • Sometimes Chest CT

    359

    CT Chest

    • More sensitive for pleural/parenchymal abnormalities
    • Best way to evaluate the mediastinum w/o sedation (TEE requires sedation)
    • Cons: Requires IV Contrast for Angiography
    • Not always available

    360

    Total CPK

    • Rises early in AMI, skeletal muscle trauma (chest trauma), aortic catastrophe, etc.
    • Very non-specific, not as sensitive as you'd like
    • If high, somethings bad

    361

    CK-MB Fraction

    • More specific for cardiac muscle damage
    • Best interpreted in the contex of CK-MB/Total CPK
    • Also elevated in brain, or w/ rhabdo/liver failure
    • Quick, cheap

    362

    Troponin

    • Much more specific for cardiac muscle
    • Doesn't explain WHY the muscle is damaged 
    • Can also be high in tachy, acute heart failure, sepsis, myocarditis, and others

    363

    BNP, or NT-ProBNP

    • Very high NPV
    • If normal, NO acute heart failure

    364

    12-Lead EKG

    • Very specific (AMI, PE [S1Q3T3], Pericarditis)
    • More specific for LVH than echo
    • NOT very sensitive

    365

    Acute Onset Chest Pain - Self Resolves

    • All studies negative
    • Needs followup - telemetry, serial enzymes, ekgs
    • Risk Stratify (TIMI, GRACE, PURSUIT) *GRACE BEST*
      • If intermediate or high risk → Cardiac Stress Test
      • If develops ST Elevation, or Enzymes Elevate → Cath

    366

    Acute Chest Pain - Resolves w/ Nitroglycerin

    • Was BP high?
    • NT-proBNP, EKG, CXR, Serial Enzymes
      • LVH, High BNP, Pulm Edema → Acute Heart Failure (Diastolic More Common); Get Echo, Control BP
      • If All Normal, and BP Not High, Risk Stratify
        • Likely needs stress test, cath if high risk
        • Consider OMM, barium swallow

    367

    Chest Pain Lasts Several Minutes, Doesn't Reproduce w/ Palpation, One (or Two) Episodes

    • EKG Normal
    • Enzymes Negative, but elevate on serial testing
      • Consider Echo
      • Arrange Stress vs. Cath

    368

    Diagnositic Considerations of Nephrolithiasis

    • Severity and Type
    • First or Recurrent?
    • Presence or absence of systemic disease and/or risk factors for recurrent stone
    • Family hx of nephrolithiasis (Significant Risk Factor)

    369

    Nephrolithiasis Presentation

    • Renal Colic
    • Hematuria
    • Asymptomatic - Most Common
    • Vague Abdominal Pain
    • Testicular Pain
    • Urinary Frequency and Urgency
    • Dysuria
    • Passage of Gravel or a Stone

    370

    Stone Passage

    • Grow on renal papillae or w/in collecting system where they do not cause symptoms
    • Become symptomatic when they pass into the ureter or occlude the uteropelvic junction
      • Usually flank pain, which spreads toward the groin, testis, vulva
      • Most stones smaller than 5mm will pass spontaneously
    • One of the more common causes of hematuria

    371

    Risk of Formation of Stone

    • Hx of Prior
      • 15% at one year, 35-40% at 5 years, 50% at 10
    • Family Hx
      • Greater than two fold increase
      • Genetic factors
    • Enhanced Enteric Oxalate Absorption
      • Gastric bypass, short bowel syndrome
    • Frequent Upper UTIs
      • Struvite stones in UTIs w/ urease producing organisms
        • Proteus and Klebsiella
    • HTN
      • Two fold increase
    • Persistently acidic urine promotes

    372

    Types of Stones

    • Calcium Salts
      • Calcium Oxalate - More Common
      • Calcium Phosphate
        • Hydroxyapatite - More Common
        • Brushite
      • 75-85% of All Stones
    • Uric Acid
    • Cystine
    • Struvite (MgNH4PO4)
    • Same patient may have more than one type of stone at the same time

    373

    Diagnosis of Stones

    • IV Pyleogram
      • Previosly the diagnostic test of choice
    • Non-Contrast Helical CT
      • TEST OF CHOICE
    • Ultrasound
      • May miss small stone
      • Good in pts who need to avoid radiation
        • Pregnant women, possible women of childbearing age
    • Abdominal Plain Film
      • Only will see radiopaque stones such as calcium, struvite, and cystine stones
      • Will miss radiolucent uric acid stones
      • Little role now that CT is available

    374

    Treatment of Stones

    • Allow Stone to Pass
      • Pain Control
      • Hydration
      • Strain Urine
    • Urology Consult
      • Consider for septic patients, acute renal failure, unrelenting pain, anuria
      • Treament w/
        • Shock wave lithotripsy
        • Percutaneous nephrolithotomy
        • Laproscopic removal
        • Ureteroscopic lithotripsy
      •  

    375

    Calcium Stones

    • Supersaturated urine w/ crystal formation and aggregation
    • More Common in MEN
    • Average age - 3rd and 4th Decade
    • Recurrence, 50% over 10 years
      • Rate of new formation is one stone every 2-3 years

    376

    Risk Factos for Calcium Stone Formation

    • Urinary
      • Lower Volume
      • Higher Calcium
      • Higher Oxalate
      • Lower Citrate
      • Higher pH
    • Anatomic
      • Medullary Sponge Kidney
      • Horseshoe Kidney
    • Diet
      • Lower Fluid Intake
      • Lower Dietary Calcium
      • Higher Oxalate Lower Potassium
      • Higher Animal Protein
      • Higher Sodium
      • Higher Sucrose
      • Lower Phytate
      • Higher Vitamin C
    • Other Medical Conditions
      • Primary Hyperparathyroidism
      • Gout
      • Obesity
      • Diabetes Mellitus

    377

    Idiopathic Hypercalciuria

    • Most common metabolic abnormality
    • Familial
      • Probably polygenic trait
      • Rare monogenic causes
        • Dent's disease; X-linked characterized by hypercalciuria, nephrocalcinosis, and progressive kidney failure
    • Hypercalciuria w/o hypercalcemia or other systemic cause of mineral dysmetabolism
    • Urinary calcium excretion greater than 250 mg/day in women and 300 mg/day in men
    • May be related to slightly higher plasma levels Vitamin D

    378

    Hyperoxaluria

    • Oxalate is a metabolic end product in humans
      • Metabolism of glycine and ascorbic acid
    • Oxalate also come from diet (40-50%)
    • Risk of calcium oxalate stone formation increases as urine oxalate excretion increases
    • Upper limit of normal is 40-50 mg/day
    • Increased dietary calcium can decrease absorbed dietary oxalate
    • Small bowel disease which results in fat malabsorption also increases oxalate absorption

    379

    Hypocitraturia

    • Inhibitor of crystal formation
      • Creates a soluble complex w/ calcium, reducing free urine calcium
    • Found in 20-40% of stone formations
    • Causes
      • Chronic metabolic acidosis
      • High animal protein diet
      • Proximal (Type I) Renal Tubular Acidosis

    380

    Hyperuricosuria

    • High urine uric acid promotes calcium stone formation
    • About 20% of stone formers
    • Excessive intake of purine from meant, fish, and poultry
    • Allopurinol has been shown effective at reducing stones in one randomized, controlled trial
      • 100 mg twice daily
    • There is probably other factors at play

    381

    Struvite Stones

    • UTI
      • Proteus
    • Urease
      • Degrades urea to NH3 and CO2
      • NH4 is created which precipitates w/ PO4 and Mg
        • Magnesium ammonium phosphate crystals form
    • Stone is usually calcium carbonate mixed w/ struvite
    • Women usually form struvite stones at a higher rate
    • Stones form rapidly over weeks
    • If not treated will create staghorn calculus
    • Passage of stones is rare

    382

    Uric Acid Stones

    • Gout
    • Idiopathic Uric Acid Lithiasis
    • Dehydration
    • Urine pH is <5.4 and often below 5.0
    • Myeloproliferative syndromes
    • Chemotherapy
      • Most are pretreated w/ allopurinol
    • Lesch-Nyhan Syndrome

    383

    Treatment of Uric Acid Stones

    • Raise Urinary pH
      • Potassium citrate or potassium bicarbonate
    • Lower excessive urine uric acid excretion
      • Allopurinol

    384

    Cystine Stones

    • Rare, autosomal recessive cause of kidney stones
    • Defective transport of dibasis aminoacids
      • Impaired renal and intestinal cystine transport
    • 10% of stones are not made of cystine
    • Detected using urine sodium nitroprusside test
    • Rarely form if urinary cystine is less than 300 mg/day

    385

    Treatment of Cystine Stones

    • High fluid intake, even at night, is the most important treatment
      • Urine volume should exceed 3 L/day
    • Low salt diet can reduce cystine excretion
    • Urinary alkalinization
    • Cystine Binding Drugs
      • Penicillamin
      • Tiopronin
      • Captopril - Best Drug
    • Invasive Therapies

    386

    Treatment of Hepatorenal Syndrome

    • General Measures
      • Antibiotics
      • Large Volume Paracentesis
      • Avoid overhydration
      • IV steroids in patients w/ sepsis and renal failure
    • FIRST LINE THERAPY
      • Albumin and Terlipressin
        • Terlipressin should not be used in pts w/ CAD, PVD, CVD
        • Discontinue treatment in 4 days in not responsive
        • ONLY continue in responders
      • If Terlipressin not available use NE or Midodrine w/ Octreotide
    • Vasopressin Analogues effective in 40-50%
      • Terlipressin (Glypressin) 0.5-1mg q 4-6hrs up to 2 mg + Albumin 1 g/kg for 2 days (max 100 g/d) then 20-40 g/d for 14 days
      • Norepineprhine + Albumin for 14 days
      • Midodrine 3 times/day w/ Octreotide + Albumin
    • Essentially, Vasopressin + Albumin
    • Titrate ALL Meds to increase MAP by 10
    • If attempt to improve renal perfusion not successful - Dopamine and Prostaglandins
    • Dialysis ONLY as bridge to transplant
    • TIPS
    • Liver Transplant

    387

    Prognosis of Hepatorenal Syndrome

    • Poor for pts w/ Cirrhosis and Renal Failure
    • Overall Survival: 50% as 1 month & 20% at 6 months
    • Hepatorenal Syndrome
      • Worse w/ Type 1

    388

    Contrast Nephrotoxicity

    • Defined as 0.5 mg/dl rise in creatinine or 25% increase in creatinine
    • May be 3rd most common cause of ARF

    389

    Rhabdomyolysis

    • Key compound is MYOGLOBIN
      • Usually bound to plasma globulins
    • Degree varies from mild rise CPK to massive increases causing ARF

    390

    Etiology of Rhabdomyolysis

    • Trauma
      • Accidents, compression muscles
    • Occlusion of muscular vessels
      • Thrombosis, embolism, clamping of vessels during surgery
    • Strainful Exercise
      • Worse in untrained and hyokalemic
      • Hot, humid conditions
      • Muscular exertion, hypoxemia, steroid myopathy in patients w/ status asthmaticus
    • Electrical Current
      • Electrical injury and lightening strikes
    • Hyperthermia
      • Neuroleptic Malignant Syndrome
        • Found in pts treated w/ phenothiazides or haloperidol
      • After anasthesia w/ halogenated hydrocarbons or succinylcholine
    • Metabolic Myopathies
    • Drugs and Toxins
      • HMG-CoA Reductase Inhibitors
        • Exacerbated by simultaneous use of danazol, nicotinic acid, cyclosporine, intraconazole, erythromycin
        • Gemfibrozil
      • Fibrates
      • Alcohol
    • Infections
    • Electrolyte Abnormalities

    391

    Pathophysiology of ARF and Rhabdomyolysis

    • Renal Vasoconstriction and Dehydration
      • Enhance water reabsorption
    • Intraluminal Cast Formation
      • Water is reabsorbed from tubules, concentrating myoglobin causing obstructing casts
      • Uric Acid also contributes to this process
    • Direct heme-protein-induced cytotoxicity

    392

    Metabolic Derangements in Rhabdomyolysis

    • Substantial fluid accumulates in affected limb
      • Must administer large amounts of fluids to prevent shock and hypernatremia
    • Dehyrdration initially causes hyperalbuminemia
      • Due to fluid, inflammation, and hyoalbuminemia
    • Metabolic acidosis 
    • Muscle Contraction and Seizures - calcium accumulation in muscles
    • Phospherous release from muscle exacerbates hypocalcemia
    • Hyperkalemia due to cell muscle release
    • Uric Acid released causing tubular obstruction

    393

    Diagnosis of Rhabdomyolysis

    • Reddish-Brown Urine w/o hematuria
    • Urine Myoglobin
    • Elevated CPK > 5000 indentifies patients at risk
    • Elevated Aldolase

    394

    Prevention and Treatment of Rhabdomyolysis

    • Treat underlying cause
    • Aggressive Fluid Resuscitation
      • IV saline should be administered ASAP after injury
        • D5W w/ 3 amps of NaBicarb
          • Keep urine pH >6.5
        • Mannitol IF patient has urinary flow
    • Prevent Factors that Cause ARF
      • Volume Depletion
      • Tubular Obstruction w/ Uric Acid Casts
    • Allopurinol
      • To reduce production of uric acid
    • Pentoxyfilline
      • Considered to enhance capillary flow, decrease neutrophil adhesion and cytokine release
    • Control HYPERKALEMIA
    • Hypocalcemia
      • Correct if severe
    • Hemodialysis
      • If necessary

    395

    Tubulointerstitial Nephritis

    • Primary TIN is comprised of diseases where the dominant pathogenic process begins in the interstitial compartment
    • Secondary TIN encompassses disease where the primary process begins in the vascular, glomerular, or collecting system, followed by damage to the interstitium

    396

    Risk Factors of Contrast Nephropathy

    • Renal Insufficiency
    • DM
    • CHF, Cirrhosis
    • Large volumes of contrast media
    • Age >75
    • Dehydration
    • Volume Depletion
    • NSAIDs
    • ACE-I

    397

    Prevention of Contrast Nephropathy

    • Initiate prevention in pts w/ GFRs of 60 ml/min
    • Saline
    • Low-Osmolality Media - pts w/ high creatinines
    • Lasix/Mannitol - Increases Risk so stop them
    • NaBicarb
    • Fenoldopine
    • NSAIDs, Diuretics, ACE, and ARB should all be discontinued 48-72 hours prior to procedure
    • D5W + 3 amps of Bicarb before exam in emergent situations

    398

    Clinical Manifestations of Contrast Nephropathy

    • Acute oliguria is uncommon
    • Gradual detioration in renal function over 3-5 days immediately after exposure
      • Returns to baseline by day 10

    399

    Nephrogenic Systemic Fibrosis

    • Occurs exclusively in patient w/ kidney failure
    • Due to gadolinium administered w/ MRIs
    • Thickening and hardeing of skin
    • Marked expansion and fibrosis of dermis w/ CD34-positive fibroblasts
    • Gadolinium
      • Less nephrotoxic than iodinated radiocontrast agents
      • Highest risk pts = ESRD and Stage 5
      • Most centers have stopped use if GFR <30 ml/min
      • Risk low if GFR b/t 30-59 ml/min
      • Risk is lowest if GFR >60 ml/min

    400

    Clinical Characteristics of Nephrogenic Systemic Fibrosis

    • Initial swelling of distal extemities, symmetrical, & bilateral 
    • Followed by thickening, induration, and hardening of skin several weeks later and move proximally
    • Distal nodules can be seen
    • Distal extremities most common site but then followed by trunk
    • Face almost never involved
    • Disease is progressive and leads to sever physical disability

    401

    Prevention Recommendations for Nephrogenic Systemic Fibrosis

    • Avoid use of gadolinium w/ GFR <30 ml/min
    • Caution if GFR is 30-60 ml/min
    • Hemodialysis daily for 3 days is administered to pts w/ ESRD

    402

    Common Clinical Finding of Tubular Interstitial Nephritis

    • Lack of significant proteinuria & hypoalbuminemia
    • Presences of sterile pyuria and WBC's casts rather than hematuria and RBC cast
    • Presence of concentrating defect resulting in polyuria and nocturia
    • Presence of other tubular defects, RTAs, salt wasting, osteomalacia due to Vitamin D deficiency

    403

    Clinical Presentation of Tubular Interstitial Nephritis

    • Abrupt onset of renal dysfunction
    • Most commonly found in hospitalized patients w/ progressive rise in creatinine
    • Acute TIN is frequently low on the list if fever, rash, eosinophilia, or eosinophiluria are not present
    • Absence of these signs is not helpful in excluding the diagnosis
    • Triad
      • Rash
      • Fever
      • Eosinophilia
      • Occurs most commonly in drug-associated TIN
    • Classical TIN occurs 10-20 days after onset of drug therapy
      • May be abrupt and occur w/in 2-3 days after rechallenge w/ drug to which was previously sensitized to
      • May also occur de novo in response to a medication previously tolerated
      • Mroe frequent in medications that are taken discontinuously

    404

    Lab Diagnosis of Tubular Interstitial Nephritis

    • Slow rise in creatinine compared to ARF from nephrotoxins, IV contrast, sepsis
    • Some electrolyte abnormalities but not dysfunction of specific tubular segments (Fanconi's)
    • UA - Leukocyte, Leukocyte Casts, RBCs
    • Sterile Urine Despite Leukocytes
    • Eosinophilia and Eosinophiluria
    • Proteinuria usually less than 1 g/day
    • Gallium Scan may be helpful
    • Ultrasound normal to enlarged w/ increased cortical echogenicity
    • GOLD STANDARD is Renal Biopsy

    405

    Treatment of Tubular Interstitial Nephritis

    • Remove offending drug
    • Renal biopsy should be performed first before starting drug therapy
      • Corticosteroid therapy w/ either Prednisone or Solu-Medrol but optimum dose or duration not defined 
        • Should be started w/in 7-14 days of azotemia due to onset of interstitial fibrosis after this time period
        • General dosing guidelines are 1 mg/kg Prednisone for 4 weeks
      • Cyclophophamide can be used if steroids fail
    • Progonosis
      • If detected early (w/in 1 week of creatinine) prognosis favorable
      • If missed for several weeks or patient is rechallenged and develops severe hypersensitivity, significant renal dysfunction can occur
      • If on biopsy, incomplete diffuse infiltration is found prognosis is better
      • 1-6% neutrophils in the infiltrate indicative of poor prognosis
      • Severity of interstitial fibrosis is most important prognostic factor

    406

    Recovery of Tubular Interstitial Nephritis

    • Two Phases
      • Initial rapid improvement in GFR (first 6-8 weeks)
      • Slow improvement over the next year
    • Final GFR correlates w/ degree of early improvement
    • Age at onset correlated inversely w/ final GFR
    • Severity of lesion correlated closely w/ final GFR
    • Gender, extrarenal manifestations, initial renal symptoms, had no significant relationship to outcome

    407

    Obesity

    • BMI > 30
    • 30% of adult population
    • Metabolic Syndrome
    • Central obesity is most important predisposing factor for insulin resistance
    • Metabolic syndrome, even in absence of hyperglycemia or diabetes and independent of hypertension, predisposes to CKD
      • Suggest that renal disease may start before the HTN or Diabetes
    • Therapy
      • Weight Loss/Increased Activity - Cornerstones
      • Agents that improve insulin sensitivity
      • Blockage of RAS (ACE or ARB)
      • HMG-CoA reductase inhibitors
      • Aggressive control of prediabetes, diabetes, and HTN

    408

    Mechanisms of Aging Kidney

    • Environmental Theory
    • Genetic Theory
    • May be combination of both

    409

    Progression of Aging Kidney

    • Young Adulthood to Middle Age - renal function remains stable
      • Slow deterioration occurs about 1% per year after 4th decade
      • Functional Decreases
        • GFR
        • Structural changes in renal vasculature
        • Proceed slowly
        • When HTN, diabetes, and renal disease present these changes occur at a more rapid rate
        • More vulnerable to drug toxicity
        • Gender is important determinate of rate of decline
          • Castration of males is protective, therefore the presence of androgens, rather than the absence of ovarian hormones promotes this age-related damage
    • Creatinine DOES NOT change w/ increasing age

    410

    Structural Renal Changes of Aging Kidney

    • Weight of kidney decreases w/ age
    • Large blood vessels show increased sclerosis
    • Renal Cysts - by age 60-69 incidence increase 10x in men and 4x in women
    • Renal Tumors
    • Nephrosclerosis
    • Glomerulosclerosis
    • Tubular Hypertrophy
    • Decreases in Nephron Number

    411

    Clinical Significance of Aging Kidney

    • Dosage adjust medication
    • Increased risk of AKI
    • increased risk of electrolyte abnormalities
    • Increased risk of renovascular disease and major cause of secondary HTN in elderly
    • Increase risk of UTI and Obstruction in Male

    412

    Tubular Function of Aging Kidney

    • Decreased Na+ excretion in response to Na+ deprivation increase susceptibility to dehydration
    • K+ handling is impaired leaving elderly more prone to drug induced hyperkalemia
    • Kidney can not maximally concentrate or dilute urine causing nocturia, hypo and hypernatremia

    413

    Endocrine Function of Aging Kidney

    • Anemia due to decreased erythropoietin, increased turnover and increased resistance
    • Decreased 1,25-dihydroxyvitamine D increases risks of falls and fractures
    • Decreased insulin clearance offset by increased resistance & decreased secretion, therefore, increased glucose intolerance

    414

    Microabluminuria and Aging Kidney

    • Early predictor of risk for developing diabetic nephropathy
    • Evidence suggests it may be a marker of cardiovascular morbidity in essential HTN
    • Glomerular permeability is not markedly changed in aging therefore frank proteinuria does not develop
    • Does develop in aging and is associated w/ a general increase in cardiovascular morbidity

    415

    Lowest Risk of Mortality in Elderly and Young is GFR of?

    45 ml/min or greater - Elderly

    75 ml/min or greater - Young