Sullivan Heart Disease

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Chapter 16 OSullivan (Heart Disease)

Coronary Artery Disease (CAD) - Most prevalent type of heart disease

Arrhythmia disturbance in electrical activity; could be BENIGN or MALIGNANT

Benign arrhythmia ex. Atrial fibrillation

Malignant arrhythmia ex. Ventricular Fibrillation, Ventricular Tachycardia

Sinus of Valsalva where the coronary arteries originate; the coronary arteries receive most of its

blood flow during diastole not systole

Autoregulation greatest influence on coronary arteriolar tone; quick response in change of

metabolism on local myocardial tissue; local effect not systemic

Cardiac Cycle Systole and Diastole

Atrial Kick last 1/3 of ventricular filling is by contraction of atrium. First 2/3 passive filling

Normal Heart Sounds

S1 Closure of Mitral and Tricuspid valve S2- closure of aortic and pulmonic valve

Systole is between S1 and s2

Diastole is between S2 and S1

Abnormal Heart Sounds

S3 also known as ventricular gallopheard in early diastole; assoc. with CHF (LVF)

S4 also known as atrial gallop heard in late diastole; assoc. with MI or Hypertension

Neurohormonal influences on heart

Beta-adrenergic receptors Sympathetic receptor of Heart; located at the sinus node within

myocardium

What are the effects of sympathetic stimulation of the heart?

- Increase Heart rate (chronotropy) and Force of contraction (Inotropy), Vasodilation of coronaryarteries

What neurotransmitter? Norepinephrine (Noradrenaline)

What are effects of sympathetic stimulation of alpha-adrenergic receptors on peripheral blood

vessels?

- Vasoconstriction and Increase in Peripheral Vascular Resistance (PVR)


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Sympathomimetics drugs that mimic sympathetic Nervous system stimulation ex. Dopamine,

epinephrine (commonly used in critical care; both drugs increase CO), Atropine (increase HR in px.s with

bradycardia)

Sympatholytics suppress Sympathetic NS

Parasymphathetic stimulation Via vagus nerve, direct impact on resting HR more than Sympathetic

stimulation

Effects of Parasympathetic stimulation: Heart rate depression, decrease force of atrial contraction and

decrease speed of conduction through A-V node

Systemic BP is product of CO and PVR

Factors that affect CO Venous pressure, HR and LV contractility

Factors that affect PVR arteriolar tone, vasoconstriction, blood viscosity

Vasomotor center CNS regulatory site for BP control; located within the medulla

Baroreceptor Reflex receptor: pressure/ stretch receptors at the internal carotid(carotid sinus) and

aortic arch; key role: short term regulation of BP not long term

Stimulus: Increase in arterial pressure Effect: Decrease sympha stimulation, Inc. parasympha

Vice versa

Mean Arterial Pressure Important in critical care (ICU); goal is keep MAP >60 mmHg; MAP is the

arterial pressure within large arteries over time (cardiac cycle).

MAP = (SBP + (2 x DBP)) / 3Example: 90/60 (90 + (2 x 60)) / 3

= 70 mmHg

What is Cardiac Output amount of blood that leaves ventricles in 1 min. Normal value 4-6 Liters/ min

Influenced by Heart rate and Stroke volume

What is Stroke Volume amount of blood that is ejected with each myocardial contraction

Influenced by 3 factors

a. Preload the amount of blood in ventricle at end of diastole, also known as left ventricle enddiastolic volume (LEVDV)

b. Contractility of ventriclesc. Afterload the force the LV must generate to overcome the pressure in the aorta and open the

aortic valve

Increase in Preload and Contractility = Increase SV

Increase in Afterload = Decrease SV

55-75% - Normal percent of preload ejected as the stroke volume


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What is the most widely used index of contractility? Ejection Fraction

What is Cardiac Index (CI)?

In critical care settings, CI is more used than CO. CI is the relationship of CO to the body surface

area expressed in meters.

CI = CO/ Body Surface area

Normal Value = 2.5 to 3.5 L/min/m 2

MVO2/ Myocardial oxygen demand

Also known as Rate Pressure Product (RPP) or Double product

Heart rate x SBP

Chronotropic Incompetence Insufficient HR response to increase VO2

Abnormal Exercise Response: 1.) Failure of systolic pressure to rise, 2.) BP >200 mmhg for systolic and

>110 mmhg for diastolic 3.) decrease in systolic bp of 10-15 mm Hg

Paroxysmal Nocturnal dyspnea dyspnea that awakens pxs from sleep but relieved at upright position;

this associated with left ventricular failure

Dressler Syndrome Post MI pericarditis

METs basic oxygen requirement at rest; 3.5 ml O2/kg/min

Persantine Thallium Test when px cannot do exercise testing because of neuromuscular limitation,

musculoskeletal problems

Levine sign patient clench fist over sternum during angina

Cardiogenic ShockAfter MI if there is not enough CO and Arterial pressure to supply organs;

Treatment: Intra-aortic balloon pump (IABP)

Negative Treppe Effect In a failing heart, increase in HR may cause decrease in force

Ectopic beatA beat that originates from a site other than the sinus node

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