Management of Cardiopulmonary Conditions PART 2

aortic sinuses of Valsalva

From where do the coronary arteries arise from?

Right atria

Right ventricle

Inferior posterior left ventricle

What 3 portions of the heart are supplied by the right main coronary artery

- Anterior LV and septum

- Lateral LV

What portions of the heart are supplied by the left main coronary artery

Left anterior (descending) interventricular artery

What artery of the heart connects the left main coronary artery to the Anterior LV and septum

Left Circumflex artery

What artery of the heart connects the left main coronary artery to the lateral LV

True

TRUE or FALSE: 70% of the left ventricle is supplied by Left anterior descending artery (septal infarctions - widowmaker)

1. SA node

2. Internodal tracts

3. AV node

4. Bundle of His

5. Left and Right Bundle Branches

6. Purkinje Fibers

What is the order of conduction by which the electrical signals in the heart travel

60-100 bpm

What is the intrinsic firing rate of the SA node

Sympathetic and Parasympathetic NS

What systems can alter the intrinsic firing rate of the SA node

slow down impulse to allow for ventricular filling (near parasympathetic innervation)

What is a primary function of the AV node

Parasympathetic nervous system

What nervous system acts as the breaks for the heart

ventricular contraction

What action denotes cardiac systole

closure of tricuspid/mitral valves (S1)

what action marks the onset of systole

ventricular relaxation

What action denotes cardiac diastole

Aortic and pulmonic valves close (S2)

what action marks the onset of diastole

- Phase 1: Ventricular filling (End of systole into diastole)

- Phase 2: Isovolumetric contraction

- Phase 3: Ejection

- Phase 4: Isovolumetric Relaxation

What are the 4 phases of the Ventricular Pressure-Volume Loop

- Ventricular filling

- End of systole into diastole

What occurs during phase 1 of the Ventricular Pressure-Volume Loop

Isovolumetric contraction

What occurs during phase 2 of the Ventricular Pressure-Volume Loop

Ejection

What occurs during phase 3 of the Ventricular Pressure-Volume Loop

Isovolumetric Relaxation

What occurs during phase 4 of the Ventricular Pressure-Volume Loop

End Systolic Volume (ESV)

The volume of blood in the ventricle after contraction

End Diastolic Volume (EDV)

The volume of blood in the ventricle after filling, prior to contraction

Stroke Volume (SV)

The volume of blood ejected during contraction; difference of EDV-ESV

cardiac output

Volume of blood ejected out of the left ventricle into systemic vasculature per minute

Heart Rate x Stroke Volume

Cardiac Output =

4-6L/min to allow adequate tissue perfusion

What is the average cardiac output

increase in CO to meet increases in O2 consumption/demand by working muscles

What happens to CO as a result of exercise

Ejection Fraction

The percent of blood ejected relative to the volume of blood in the ventricle prior to contraction; quotient of SV/EDV

SV/EDV

Ejection Fraction =

True

TRUE or FALSE: Ejection Fraction is the best indicator of cardiac function/ strength of cardiac contraction

55-70%

What is a normal Ejection Fraction

- Adrenal medulla (Epinephrine)

- Sympathetic chain (Norepinephrine)

What parts of the sympathetic nervous system are responsible for increasing HR (positive chronotropy)

Vagus nerve (Acetylcholine)

What parts of the Parasympathetic nervous system are responsible for decreasing HR (negative chronotropy)

NE on beta 1 receptors

What neurotransmitter and receptors act on the heart to induce positive chronotropy

Ach on muscarinic receptors

What neurotransmitter and receptors act on the heart to induce negative chronotropy

vasodilation; improved supply of blood to heart and increased cardiac contraction (increased inotropy)

vasoconstriction; decreased blood supply and dampened cardiac contractility (decreased inotropy)

Sympathetic → coronary artery _______ → ___________________

Parasympathetic → coronary artery ______ → _________________________

- Preload

- Contractility

- Afterload

What 3 factors affect the regulation of stroke volume

Preload

- The amount of stretch on the myocardial wall before contraction

- A measure of the amount of blood returning to the heart

Afterload

- Pressure that the heart must pump against

- Total peripheral resistance

True

TRUE or FALSE: Preload = EDV or venous return

capacitance vessels

What type of vessels are veins classified as

- Total blood volume

- Pressure in the venous vasculature

What is the rate of venous return dictated by

- Pressure gradient

- Muscle pumping

- Positioning

What mediums allow blood to return to the heart

right side

what side of the heart do veins return blood to?

compliance and distension

Veins have thin walls and decreased musculature in comparison to arteries; thus, increased ______ and ______

Mean venous pressure is 2mmHg (highest in most distal venules at ~10mmHg, lowest where vena cava enter atrium at 0mmHg)

What is a key point about venous pressure gradients

- Frank-Starling effect

- Force-frequency relationship

What relationships act as intrinsic controls of contractility

sympathoadrenal system (epi/norepi)

What extrinsic system acts to regulate contractility

strength of ventricular contraction increases as the pre-contractile length of myocardial cell length increases, up to a certain amount

Greater amount of blood is returned to the heart (EDV)= greater amount of blood is ejected in systole

What is the Frank-Starling effect

increased stretch on myocardial wall → increased EF

In a healthy individual with normal contractility, increased preload =

afterload

The pressure that the heart must pump against

• ESV

• Frank Starling

• contractility and hypertrophy

Afterload

• Less ejected due to resistance → increased _____ → _______ compensation → increased _____ and _____

increase in HR leads to increased contractility (if >120bpm, more Ca2+ available for excitation, contraction, and stronger contraction)

What is the Force-frequency relationship

If less blood is ejected due to resistance, more is retained in the ventricle, triggers Frank starling; increased contraction creates compensatory increase myocardial size (hypertrophy)

How can afterload impact preload

blood pressure

heart rate

how do we monitor cardiac output clinically

- Preload

- Afterload

- Contractility

What are factors that have an effect on Stroke Volume

- End Systolic Volume

- Venous Return

What are factors that have an effect on Preload

- Aortic Pressure

- Aortic Valvular Function

What are factors that have an effect on Afterload

- End Diastolic Volume

- Sympathetic Stimulation

- Myocardial Oxygen Supply

What are factors that have an effect on Contractility

- BP decreases due to changes in positions

- CO decreases

- Gravity changes preload deceasing it due to decrease in venous return this is why we have patients exercise or lay back down or compression stockings to bring blood back up to the heart and increase preload

- Exercise triggers sympathetic NS > resulting in vasoconstriction > increased resistance > increased afterload

What are key points about Orthostatic hypotension and Cardiac function

- Decreased preload

- Decreased CO

What are key points about the Valsalva maneuver and Cardiac function

Positional change > gravity causes blood to pool in LE > decreased preload > decreased stroke volume > increased HR

What are key points about POTS and Cardiac function

Rush of parasympathetic > HR decreases > blood vessels dilate > decreases preload > decreased CO

What are key points about Vasovagal Syncope and Cardiac function

Flow = ΔP/R

What is Ohm's Law

- Synthesize substances that can locally increase or decrease vascular tone and resistance

- Respond to extrinsic circulating hormones/factors

How do endothelial cells contribute to the intrinsic control of blood flow

Endothelial-derived relaxing factor (such as nitric oxide)

What are synthesized substances by endothelial cells that can locally increase or decrease vascular tone and resistance

Potent vasodilator released in response to chemical and physical stimuli; often in response to shear stress

what is the function of nitric oxide on blood flow

nitric oxide

what synthesized substance by endothelial cells are potent vasodilator released in response to chemical and physical stimuli; often in response to shear stress

endothelin

what synthesized substance by endothelial cells are vasoconstrictors released in response to endothelial damage (tearing/crushing vessels, exposure to chemicals) to prevent excessive bleeding

endothelin

A Vasoconstrictor released in response to endothelial damage (tearing/crushing vessels, exposure to chemicals) to prevent excessive bleeding

- Norepinephrine

- Epinephrine

- Angiotensin II

- Vasopressin

What substances act on the extrinsic control of blood flow by causing Vasoconstriction

- Bradykinin

- Histamine

What substances act on the extrinsic control of blood flow by causing Vasodilation

Sympathetic NS shunts blood to working muscles, diverts away from organs

What is the bodies general Physiologic Response to Exercise

Sympathetic nerve fibers stimulate alpha-adrenergic receptors → release norepinephrine → vasoconstriction

What is the bodies general Physiologic Response to Exercise at the organs

Circulating epinephrine stimulate of beta-adrenergic receptors of the working muscles → vasodilation

What is the bodies general Physiologic Response to Exercise at the muscles

Active Hyperemia

Blood flow to the organ is proportional to its metabolic activity

Metabolites from metabolic activity produce local vasodilation

What happens during Active Hyperemia

Lactate, adenosine, potassium, CO2

What metabolites form from metabolic activity that we are concerned with during active hyperemia

- ↑ in blood flow in response to a prior period of ↓ blood flow/occlusion

- During occlusion, O2 debt is accumulated followed by vasodilation until debt is paid

What happens during Reactive Hyperemia

Blood flow restriction therapy, coronary arteries

What is an example of Reactive Hyperemia

- LV thickness

- Vascular thickness

What are cardiovascular factors that increase due to normal aging

- Maximal HR

- Cardiac output

- VO2 max

- Decrease max HR

- Decrease stroke volume

- Compromised O2 uptake

- Rate of ventricular filling

What are cardiovascular factors that decrease due to normal aging

blood pressure

The force of blood pushing against the walls of the arteries

0= absent

1= weak

2+= normal

3= little bounding

4= bounding

Name the different grades of pulse rates

CO x TPR

BP =

total peripheral resistance

________ increases are the main cause of high blood pressure

- Elevated (120-129/<80)

- Stage 1 (130-139/80-89)

- Stage 2 (140+/90+)

- Hypertensive crisis (180+/120+)

What are the classifications of severity for HTN

Labile HTN

BP is sometimes elevated and sometimes normal

Malignant HTN

A blood pressue greater than 180/120 , presenting with papilledema and end-organ damage

increases Afterload

How does HTN impact cardiac function?

- Left ventricular hypertrophy (LVH)

- Decreased stroke volume

- Untreated, can lead to decreased CO (LV failure)

What are the effects of hypertensive disease or increased afterload on the heart

- decreased compliance of LV

- LVH alters myocardial oxygen demand → predisposition for ischemia

What are the consequences of left ventricular hypertrophy and diastolic dysfunction on left ventricular function

Lifestyle modification

How do we treat elevated BP (120-129 systolic AND <80 diastolic)

- If no current or high 10-year CVD risk: Lifestyle modification

- If high 10-year CVD risk: Lifestyle modification and medication

- medications: thiazide diuretics, ACE inhibitors/angiotensin II inhibitors, calcium channel blockers

How do we treat Stage 1 HTN (130-139 systolic OR 80-89 diastolic)

- Lifestyle modification and two-drug combination of BP medications

- medications need to be from 2 different classes

How do we treat Stage 2 HTN (>/= 140 systolic OR >/= 90 diastolic)

- Resting SBP >200mmHg

- Resting DBP >100mmHg

When is physician clearance needed for patients with HTN to engage in exercise testing

- SBP >250mmHg

- DBP >115 mmHg

During exercise testing for patients with HTN, what are indications to discontinue testing

Endurance training at moderate intensity

What are Aerobic Guidelines for Exercise with HTN

- Low weights, high repetitions in deconditioned/high risk

- 60-80% 1RM for all others

What are Resistance training Guidelines for Exercise with HTN

Avoid Valsalva/breath holding

What is a general exercise guideline recommendation for exercise with HTN