Coronary arteries 1 25.2.2016 . O 2 regimen of the heart TDP of - - PDF document

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Coronary arteries 1 25.2.2016 . O 2 regimen of the heart TDP of - - PDF document

25.2.2016 . Coronary Artery Disease (CAD) Arterial Hypertension Blagoi Marinov, MD, PhD Pathophysiology Dept. Medical University of Plovdiv Coronary arteries 1 25.2.2016 . O 2 regimen of the heart TDP of left Coronary ventricle


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25.2.2016 г. 1

Coronary Artery Disease (CAD) Arterial Hypertension

Blagoi Marinov, MD, PhD Pathophysiology Dept. Medical University of Plovdiv

Coronary arteries

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25.2.2016 г. 2

O2 regimen of the heart

О2 requirements О2 delivery

Heart rate Contractile state Wall stress О2 extraction О2 content Coronary blood flow TDP of left ventricle Coronary resistance

Atherosclerosis – the most important etiologic factor

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Risk factors for Atherosclerosis

Major Lesser, Uncertain, or Nonquantitated Nonmodifiable Increasing age Obesity Male gender Physical inactivity Family history Stress ("type A" personality) Genetic abnormalities Postmenopausal estrogen deficiency High carbohydrate intake Potentially Controllable Hyperlipidemia Alcohol Hypertension Lipoprotein Lp(a) Cigarette smoking Hardened (trans)unsaturated fat intake Diabetes Chlamydia pneumoniae

Pathogenetic events, and clinical complications of atherosclerosis in the coronary arteries

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Definition

Ischemia refers to an insufficient amount

  • f blood. Since the coronary arteries are

the only source of blood for the heart muscle its blood supply will suffer tremendously.

Myocardial Ischemia

Myocardium becomes ischemic within 10 seconds of coronary occlusion Working cells remain viable for up to 20 minutes

– Anaerobic mechanisms kick in

Lactic acid Free radical damage, especially after reperfusion

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25.2.2016 г. 5

Ischemic episode

Severity Duration Frequency

Pain Ischemia

CAD classification

Stable angina Unstable angina Atypical angina (Prinzmetal) Myocardial infarction Atherosclerotic myocardiosclerosis Silent ischemia Sudden cardiac death

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Stable angina

Chest pain with exertion

May radiate, may have diaphoresis, SOB, pallor Relief with rest or nitrates Increased О2 demand Decreased О2 delivery

Morphological substrate

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Treatment for Stable Angina

Drug

– Nitrates – Beta blockers – Calcium Channel Blockers – Statins

Invasive cardiology

– PTCA – Stent

Surgery

– Bypass

Acute Coronary Syndrome

Atherosclerotic Plaque Stable Plaque Unstable Plaque Stable Angina Acute Coronary Syndrome Sustained Ischemia Myocardial Infarction Transient Ischemia/ Unstable Angina Necrosis

Frequency Severity Magnitude Duration

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atherosclerotic plaque blood clot sticking to plaque narrowed lumen

Advances in interventional cardiology

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PTCA: Percutaneous Transluminal Coronary Angioplasty

Invasive, but nonsurgical technique to reduce frequency and severity of chest discomfort

  • May also be used during evolving MI

Procedure performed under fluoroscopic guidance in cardiac cath lab

  • Balloon inflation may be repeated until lesion is

reduced or eliminated

  • Stents may be placed at time of procedure

CABG: Coronary Artery Bypass Graft

Most common cardiac surgery Indicated for patients who do not respond to medical management of CAD or when disease progression is evident To be bypassed vessels should have proximal lesions with > 70% occlusion Most effective when good ventricular function remains and ejection fraction is more than 40- 50% Requires Cardiopulmonary bypass during surgery

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Myocardial infarction (MI)

Transmural Non-transmural (subendocardial, without Q wave) Ischemic necrosis of the part of myocardium (more frequently on the left).

General characteristics

  • Myocardium becomes hypoxic
  • Shift to Anaerobic Respiration
  • Waste products release/hypoxic injury
  • Cardiac output impaired

Pathogenesis of MI

Time !

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25.2.2016 г. 11

Myocardial Changes

Myocardial stunning

– Temporary loss of contractility that persists for hours to days

Myocardial hibernation

– Chronically ischemic; myocytes are hibernating to preserve function until perfusion can be restored

Myocardial remodelling

– Loss of contractility mediated by Ang II, catecholamines, and inflammatory cytokines

Signs and symptoms of MI

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ECG changes

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Change in serum enzymes

Immediate Post MI Tx

Reduce myocardial workload Prevent Remodeling Reduce chances of reocclusion Reduce oxidative stress (reperfusion injury)

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Long-term Post MI Treatment

Lifestyle

– Diet – Exercise – Cardiac Rehab – Stress management

Drugs

– Antiplatelet: aspirin, clopidogrel – Beta blocker – Statin medication – Treat risk factors (HTN, lipid, smoke, etc.)

Complications of MI

Disorders of rhythm and conduction

  • Supraventricular
  • Ventricular (tachicardia, fibrillations)

Rupture of post infarction aneurism Pericarditis (Dressler syndrome) Post infarction angina (20-30 %)

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Prognosis of MI

Acute MI is associated with a 30% mortality rate; half of the deaths occur prior to arrival at the hospital. An additional 5-10% of survivors die within the first year after their MI. Approximately half of all patients with an MI are rehospitalized within 1 year of their index event. Overall, prognosis is highly variable and depends largely

  • n the extent of the infarct, the residual LV function, and

whether the patient underwent revascularization.

Screening of different forms

  • f CAD

Stress test Coronary angiography Electro- cardiogram

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25.2.2016 г. 16

ARTERIAL HYPERTENSION

Blood pressure levels*

Systolic Diastolic Level 120 80 Optimal < 130 < 85 Normal 130-139 85- 89 Normal borderline 140 -159 90 - 99 Mild hypertension 160-179 100-109 Moderate hypertension > 179 > 109 Severe hypertension > 140 < 90 Maximum or systolic hypertension

*Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and treatment of High Blood Pressure

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Cardiac output and peripheral resistance in blood pressure regulation

The burden of hypertension

(distribution by age and sex*)

*CDC. National Health Survey, 2005

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Types of Hypertension

 Essential Hypertension (Primary)  Secondary Hypertension

Risk factors for arterial hypertension

Primary

  • NaCl rich diet
  • Stress

Secondary

 Hypercholesterolemia

 Prediabetic state  Overweight  Sedentary lifestyle  Alcohol abuse

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Medium caliber arteries are the most affected

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Genetic background Pathogenesis of Hypertension

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Pathogenetic units for arterial hypertension

Endocrine

Hypothalamo- pituitary axis

Neurogenic

Pressor dominance in CNS Sympathetic nervous system

Renal

 RAAS  Renal depressor system

Cardiovascular

 Total peripheral resistance (TPR) Hypervolemia  Cardiac output (CO)

Symptoms and signs

Almost always asymptomatic Dyspnea most common Headache,Dizziness,Tinnitus,Fainting not correlated with hypertension Symptoms poorly correlated to degree of hypertension

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25.2.2016 г. 23

Consequence of HTN

(CHF)

Staging of arterial hypertension

Labile hypertension

Increased CO Normal TPR

Stable hypertension

Increased TPR Normal CO

Organ damage and complications

Compensated Decompensated

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25.2.2016 г. 24

Complications of Hypertension It can always get worse …

Renal Acute glomerulonephritis Chronic renal disease Polycystic disease Renal artery stenosis Renal artery fibromuscular dysplasia Renal vasculitis Renin-producing tumors Endocrine Adrenocortical hyperfunction Exogenous hormones Sympathomimetics, Pheochromocytoma Acromegaly Hypothyroidism (myxedema) Hyperthyroidism (thyrotoxicosis) Pregnancy-induced Cardiovascular Coarctation of aorta Polyarteritis nodosa (or other vasculitis) Increased intravascular volume Increased cardiac output Rigidity of the aorta Neurologic (Psychogenic) Increased intracranial pressure Sleep apnea Acute stress, including surgery

Secondary Hypertension

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25.2.2016 г. 25

Antihypertensive Agents

General Classes of Agents:

  • Diuretics
  • Sympatholytic agents
  •  blockers (central)
  •  blockers (peripheral)
  • Vasodilators
  • Agents which interfere with the RAAS
  • ACE inhibitors
  • Angiotensin receptor blockers

Thank you !