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Cardiac Patient Assessment & Treatment

This review provides information on cardiac output, vital signs, and acquired heart diseases such as angina pectoris, myocardial ischemia, myocardial infarction, and congestive heart failure. It covers the physiology, symptoms, and treatment of these conditions, as well as the assessment of cardiac enzymes and left ventricular failure.

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Cardiac Patient Assessment & Treatment

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  1. Cardiac Patient Assessment & Treatment

  2. Review: • Cardiac Output • 5000-6000 ml/min. • HR or SV = CO • Sympathetic effects: • HR and SV • Parasympathetic: • Slows HR • Little effect on SV

  3. Review: • SV = pressure in ventricle • Frank Starling effect • Peripheral vascular constriction increases venous return • = Increased RV output. • Vasodilation of arteries decreases PVR and diastolic pressure • = Increased CO.

  4. Vital Signs • Normal B/P is 120/70 mmHg • Increases with age • General: • Systolic – 100 + age up to 140 • At age 50: usually 140 mmHg • Increases 1 mmHg/yr after 50.

  5. Dispatched as: Man down Chest pain Heart attack SOB Fainted Dizzy Passed out Choking Stroke DFO DRT Abnormal Cardiac Function

  6. Brief History Onset Provoking factors Quality Radiation Severity Time BP changes Initial Assessment:

  7. Initial Assessment • Meds • Cardiac rhythm • Abnormal breathing • Edema • Rales • Changes in skin color and moisture

  8. Acquired heart diseases (Not Congenital) • Angina Pectoris • Myocardial Ischemia • Myocardial Infarction • Cardiogenic Shock • Cor Pulmonale • Hypertension

  9. Angina Pectoris • Physiology: • Myocardial Demands not met • Stable • Onset with exertion • Subsides with rest within 5 minutes • If onset with stress, pain may last 15 min.

  10. Angina Pectoris • S/S: • Heavy squeezing pressure with radiation • Anxious • Diaphoretic • Clammy • SOB

  11. Angina Pectoris • Unstable • In patients with previously stable angina • Frequency, Severity & Duration • Pain with less activity or at rest. • More resistant to relief with NTG.

  12. Myocardial Ischemia • Physiology: • Similar but worse • Occurs anytime • Can last 30-60 minutes • Not permanent damage • May fail acutely or fibrillate

  13. Myocardial Ischemia • S/S • Tachycardia • Elevated systolic BP • Transient (Brief) ST depression • Possible T wave inversion • Precursor to …

  14. Myocardial Infarction • Physiology: Coronary ThrombusArteriosclerosis / Atherosclerosis • History: (**) • CP • Possible Radiation • Sweating • Nausea • SOB • Pallor

  15. AMI - Another Rhythm? • Circadian rhythm • 3x more likely in AM • Usually 3-4 hrs. after awakening. • CP awakened from sleep

  16. AMI • Note: • Elders & Diabetics often have no pain • History: • General Malaise • Burning • Syncope • Dizziness

  17. AMI History • Nausea • Diaphoresis • Weakness, unknown fatigue • Hot flash • Nonspecific chest discomfort • CHF; rales

  18. AMI History • Intermittent sx • Seasonal - fall and winter • MI at rest - no precipitating factors

  19. AMI HUGE Risk Factors • 2x more likely to die in 1st year post MI • Increased stroke risk • 1/2 > 75 y/o • PMHx: HTN, Diabetes

  20. AMI Little Known Fact-Cliff Claven • Socialization key clue (Females) • Significantly less likely to be referred to cardiac cath lab, thrombolytics, or angioplasty • ** Increase index of suspicion

  21. Treatment of AMI • Treatments, as always, are based on Symptoms • Ectopy • Pain • Coronary Perfusion • Container Problem • Fluid (mis)placement problem

  22. Hospital Assessment of AMI • Cardiac Enzymes • Qualitative CPK (Creatine phosphokinase) • CK-MB: :0 – 4 • PEAK 12-24 H • Troponin: 0 – 0.1 • ONSET 1 – 4 H • PEAK 12-24 H • Significant ECG Changes • Symptoms within 24 hours • History (Surgeries) • Candidate for Thrombolytics?

  23. Acute Left Ventricular Failure • Acute LVF from heart disease: • #1 cause of heart failure. • Assume the worst, hope for best • Pt. with CAD w/ hx of MI (new or old) • May develop LVF. • Frequently LVF is only manifestation of AMI.

  24. LVF • Common causes • Systemic HTN • Afterload • Coronary artery disease • Arteriosclerosis/atherosclerosis • Ischemia • Local/temporary occlusion

  25. LVF • Common Causes • Infarction • Permanent, necrosis • Significant Sized Infarct • Decrease effective wall motion • Decreased stroke volume • Cardiomyopathy • Diseased heart muscle tissue • ETOH • Enlargement

  26. LVF • Causes • Volume overload • Bag of Potato Chips • Severe anemia • Hypoxemia

  27. LVF and Pulmonary Edema • Incidence of CHF doubles per decade of life • CO falls and pulmonary capillary pressure rises. • Fluid move (interstitial & alveolar) • Lymphatic system fails to remove/filter.

  28. CHF • Acute CHF • Rapid • Chronic CHF • Slow • Midnight shoppers

  29. Pulmonary edema results from: • CVA • Pulmonary embolism • Infection - Sepsis • Allergy • Inhalation of fumes • Narcotic abuse • Especially Inhaled (Heroin) • Altitude sickness.

  30. Generalized weakness Fatigue Dyspnea Cyanosis Tachycardia JVD – Indirect Increase B/P & Pulse Chest pain Agitation Anxiety Pulmonary Edema – S/S

  31. Pulmonary Edema – S/S • Tachypnea • Orthopnea • Paroxysmal Nocturnal Dyspnea • Elevation of pulmonary venous & cap pressures • Wakening from sleep

  32. Noisy Labored Breathing Rales Wheezes Reflex airway spasm “Cardiac asthma” Rhonchi (larger airways) Coughing Blood Tinged Sputum Pink Frothy Pulmonary Edema – S/S

  33. Cardiogenic Shock • LV function compromised and CO falls • S/S - Decompensating • Systolic BP < 80 mmHg • Usually semiconscious • Cold, clammy skin • Mild to moderate cyanosis of lips and nail beds. • EKG usually sinus tach

  34. Cardiogenic Shock • Note: If pt appears dehydrated • (neck veins flat) • Suspect hypovolemia. • Fluid Resuscitation? Or Not? • Hmmmmmmmmm.

  35. Right Ventricle Failure • Leading Cause • LVF • MI’s & HTN mostly affect LV • Isolated RVF • Pulmonary HTN & Cor Pulmonale • RA / RV Infarct (Rare) • Pulmonary and Mitral valve stenosis • Pulmonary vascular HTN

  36. RVF – Physiology • Preload High • RV cannot keep up • Increased pressure in Big Veins • Max stretch & density reached • Backflow in systemic circulation • Fluid forced to interstitial spaces

  37. RVF – S/S • Neck Veins • Semi-fowlers position (45 Degrees) • Peripheral Edema • Dependent edema • Pitting edema • Sacral (bedridden) • Fluid Collection • Ascites • Pleural Effusion • Pericardial Effusion

  38. RVF – S/S • Clubbing of fingers • Chronic Hypoxia with RHF • Most of the other LVF S/S also • Cor Pulmonale • SOB • Tachypnea • Anxiety • Etc…

  39. RVF – S/S • Liver Engorgement • Big Belly (uneven to the right) – Suspect • Hx of MI • Lasix • Digoxin • “Enlarged Heart” • “Weak Heart” • “Bum Ticker”

  40. Cor Pulmonale • Hypertrophy of RV 2nd to Resp Disorder • Acute PE 2nd to clot (R Heart) • Clot / Occlusion • Increase in pulmonary vascular resistance • COPD Patients • (High Right Heart Workload, High Risk)

  41. Cor Pulmonale S/S • Sudden onset unexplained SOB • Difficulty breathing • HR elevated • Chest pain with cough • Dyspnea not aggravated by lying flat • Cold • Diaphoretic • Cyanotic • Neck veins may be distended

  42. Cor Pulmonale – Case • 58 yo male • Hx of chronic bronchitis or emphysema • Typical S/S of bronchitis • Progression • Deterioration of pulmonary capillaries • Alveolar fibrosis • Chronic hypoxemia

  43. Cor Pulmonale – Case • Progression • Increase in pulmonary artery pressures • Result RV afterload increase • RV ill equipped • RV Enlarges (Hypertrophy) • Chronic RH HTN leads to RVF

  44. Cor Pulmonale – Case • Patient displays all signs of: • RVF • Initial cause was pulmonary condition

  45. Hypertension • Defined as BP > 150/90 mmHg. • Precise cause unknown for 90% pt. • Acute Life-threatening Hypertension

  46. S/S – Hypertensive Crisis • Recent onset of H/A • Altered mental status • Signs of CHF • BP usually > 200/120

  47. So, What to do? • Decide – Sick/NotSick? • Vitals • Look • Skin – wet/dry, color, temp • JVD • Peripheral edema • Subtle signs

  48. Listen • Breath sounds • Bruit • Pulse x 6 • Skin

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