1. Cardiac Pathophysiology

2. Pericarditis Often local manifestation of another disease
May present as:
Acute pericarditis
Pericardial effusion
Constrictive pericarditis

3. Acute Pericarditis Acute inflammation of the pericardium
Cause often unknown, but commonly caused by infection, uremia, neoplasm, myocardial infarction, surgery or trauma.
Membranes become inflamed and roughened, and exudate may develop

4. Symptoms:
Sudden onset of severe chest pain that becomes worse with respiratory movements and with lying down.
Generally felt in the anterior chest, but pain may radiate to the back.
May be confused initially with acute myocardial infarction
Also report dysphagia, restlessness, irritability, anxiety, weakness and malaise

5. Signs Often present with low grade fever and sinus tachycardia
Friction rub (sandpaper sound) may be heard at cardiac apex and left sternal border and is diagnostic for pericarditis (but may be intermittent)
ECG changes reflect inflammatory process through PR segment depression and ST segment elevation.

7. Treatment Treat symptoms Look for underlying cause
If pericardial effusion develops, aspirate excess fluid
Acute pericarditis is usually self-limiting, but can progress to chronic constrictive pericarditis

8. Heart failure
Definition – When heart as a pump is insufficient to meet the metabolic requirements of tissues.
Acute heart failure
65% survival rate
Chronic heart failure
Most common cause is ischemic heart disease

9. Ischemic Heart Disease
Coronary Artery Disease (CAD), myocardial ischemia and myocardial infarction are progression of conditions that impair the pumping ability of the heart by depriving it of oxygen and nutrients.

10. Coronary Artery Disease
Any vascular disorder that narrows or occludes the coronary arteries.
Most common cause is atherosclerosis

11. The arteries that supply the heart are the first branches off the aorta
Coronary artery disease decreases the blood flow to the cardiac muscle.
Persistent ischemia or complete occlusion leads to hypoxia.
Hypoxia can cause tissue death or infarction, which is a “heart attack,” which accounts for about one third of all deaths in U.S.

12. Risk Factors Hyperlipidemia Hypertension Diabetes mellitus
Genetic predisposition
Cigarette smoking
Obesity
Sedentary life-style
Heavy alcohol consumption
Higher risk for males than premenopausal women

13. Myocardial Ischemia Myocardial cell metabolic demands not met
Time frame of coronary blockage:
10 seconds following coronary block
Decreased strength of contractions
Abnormal hemodynamics
See a shift in metabolism, so within minutes:
Anaerobic metabolism takes over
Get build-up of lactic acid, which is toxic within the cell
Electrolyte imbalances
Loss of contractibility

14. 20 minutes after blockage
Myocytes are still viable, so
If blood flow is restored, and increased aerobic metabolism, and cell repair,
→Increased contractility
About minutes after blockage, if no relief
Cardiac infarct & cell death

15. Clinical Manifestations
May hear extra, rapid heart sounds
ECG changes:
T wave inversion
ST segment depression

16. Chest Pain First symptom of those suffering myocardial ischemia.
Called angina pectoris (angina – “pain”)
Feeling of heaviness, pressure
Moderate to severe
In substernal area
Often mistaken for indigestion
May radiate to neck, jaw, left arm/ shoulder

17. Three types of angina pectoris:
Due to :
Accumulation of lactic acid in myocytes or
Stretching of myocytes
Three types of angina pectoris:
Stable, unstable and Prinzmetal

18. Stable angina pectoris
Caused by chronic coronary obstruction
Recurrent predictable chest pain
Gradual narrowing and hardening of vessels so that they cannot dilate in response to increased demand of physical exertion or emotional stress
Lasts approx. 3-5 minutes
Relieved by rest and nitrates

19. Prinzmetal angia pectoris (Variant angina)
Caused by abnormal vasospasm of normal vessels (15%) or near atherosclerotic narrowing (85%)
Occurs unpredictably and almost exclusively at rest.
Often occurs at night during REM sleep
May result from hyperactivity of sympathetic nervous system, increased calcium flux in muscle or impaired production of prostaglandin

20. Unstable Angina pectoris
Lasts more than 20 minutes at rest, or rapid worsening of a pre-existing angina
May indicate a progression to M.I.

21. Silent Ischemia Totally asymptomatic
May be due abnormality in innervation
Or due to lower level of inflammatory cytokines

22. Treatment Nitrates dilate peripheral blood vessels and
Pharmacologically manipulate blood pressure, heart rate, and contractility to decrease oxygen demands
Nitrates dilate peripheral blood vessels and
Decrease oxygen demand
Increase oxygen supply
Relieve coronary spasm

23.  blockers:
Block sympathetic input, so
Decrease heart rate, so
Decrease oxygen demand
Digitalis
Increases the force of contraction
Calcium channel blockers
Antiplatelet agents (aspirin, etc.)

24. Surgical treatment Angioplasty – mechanical opening of vessels
Revascularization – bypass
Replace or shut around occluded vessels

25. Myocardial infarction
Necrosis of cardiac myocytes
Irreversible
Commonly affects left ventricle
Follows after more than 20 minutes of ischemia

26. Structural, functional changes
Decreased contractility
Decreased LV compliance
Decreased stroke volume
Dysrhythmias
Inflammatory response is severe
Scarring results –
Strong, but stiff; can’t contract like healthy cells

27. Clinical manifestations
Sudden, severe chest pain
Similar to pain with ischemia, but stronger
Not relieved by nitrates
Radiates to neck, jaw, shoulder, left arm
Indigestion, nausea, vomiting
Fatigue, weakness, anxiety, restlessness and feelings of impending doom.
Abnormal heart sounds possible (S3,S4)

28. Blood test show several markers:
Leukocytosis
Increased blood sugar
Increased plasma enzymes
Creatine kinase
Lactic dehydrogenase
Aspartate aminotransferase (AST or SGOT)
Cardiac-specific troponin

29. ECG changes Pronounced, persisting Q waves ST elevation
T wave inversion

30. Treatment First 24 hours crucial Hospitalization, bed rest
ECG monitoring for arrhythmias
Pain relief (morphine, nitroglycerin)
Thrombolytics to break down clots
Administer oxygen
Revascularization interventions: by-pass grafts, stents or balloon angioplasty

31. Atherosclerosis
A form of arteriosclerosis where soft deposits of intra-arterial fat and fibrin harden over time – atheroma
May see build up in skin – Xanthoma or arcus in cornea.
In general, patients suffer few symptoms unless > 60 % of blood supply is blocked

32. Progressive over years
Starts with some injury to endothelium
Smoking, hypertension, hyperlipidemia, diabetes, autoimmune disease, and infection
Inflammation, release of enzymes by macrophages causes oxidation of LDL, which is then consumed by macrophages – foam cells – accumulate to form fatty streaks
Fatty streaks of lipid material appear first as yellow streaks and spots
Smooth muscle cells proliferate, and migrate over the streak forming a fibrous plaque

33. Fibrous plaque results in necrosis of underlying tissue and narrowing of lumen
Inflammation can result in ulceration and rupture of the plaque, resulting in platelet adherence to the lesion = complicated lesion
Can result in rapid thrombus formation with complete vessel occlusion → tissue ischemia and infarction

36. Clinical manifestations
Signs and symptoms of inadequate perfusion – TIAs, often associated with exercise or stress
When lesion becomes complicated, can result in tissue infarction
Coronary artery disease – myocardial ischemia
In brain – major cause of stroke

37. Treatment Exercise Smoking cessation
Control of hypertension and/ or diabetes
Reduce LDL cholesterol by diet or medication or both

38. Other arterial problems
Aneurism – dilation in the arterial wall
Most arise in aorta or major branches as a result of atherosclerotic wall damage
Males over 50 at greatest risk for aortic aneurysms
Disturbs blood flow, predisposing to thrombus formation - can release thromoemboli

39. Asymptomatic until rupture
Embolism
Death
Treatment by surgical repair
Aortic Dissection –bleeding into vessel wall, separating vessel layers
Men in y.o. age group with hypertension
Younger persons with connective tissue disease or congenital defects
Presents with pain – life threatening

40. Systemic Hypertension
A consistent increase in arterial blood pressure caused by increased Cardiac output or increased peripheral resistance or both
Leads to damage of vessel walls
If arteries constrict over a long time with increased pressure in vessel, the wall becomes thicker to withstand the stress.
Results in narrowing of arterial lumen
Leads to inflammatory response

41. Causes one in eight deaths worldwide
Third leading cause of death in the world
Affects 50 million Americans

42. Primary hypertension Also called essential or idiopathic hypertension
% of all cases
No specific cause identified
Can happen with retention of sodium and water → increased blood volume.
Also low dietary potassium, calcium and magnesium intakes

43. Other risk factors Smoking Nicotine is a vasoconstrictor
Greater than 3 alcoholic drinks/ day
2-4 drinks / week lowers blood pressure

44. Suspected causes Interaction of genetics and environment
Overactivity of sympathetic nervous system
Overactivity of renin / angiotensin/ aldosterone system
Salt and water retention by kidneys
And others

45. Secondary hypertension
Caused by a systemic disease process that raises peripheral resistance or cardiac output = % of cases.
Renal vascular disease
Adrenocortical tumors
Adrenomedullary tumors
Drugs ( oral contraceptives, corticosteroids, antihistamines)

46. Complicated hypertension
Sustained primary hypertension that damages the structure and function of the vessels themselves.
Commonly affects heart, aorta, kidneys, eyes, brain, and lower extremities (target-organ damage).

47. Clinical manifestations
None in early stages other than elevated BP
Some individuals never have symptoms; others become very ill and die

48. Treatment Modification of life style Drugs
Diuretics, beta-blockers, angiotensin converting enzyme inhibitor
Compliance is often difficult – patients stop taking medication when they feel better – can get rebound effects

49. Venous Disorders
Varicose veins – dilations, can lead to valvular insufficiency
Can occur in superficial veins (saphenous) or deep veins
Causes of secondary varicose veins:
Deep vein thrombosis
Congenital defects and pressure on abdominal veins