below L₀

total tension is dependent on active tension below L₀

negative: PNS, CHF, ACh

positive: SNS, ↑HR, cAMP, β₁ agonists, cardiac glycosides (eg. digoxin)

Arteriosclerosis: ↑ in SP, PP and MAP

↓ in arterial compliance

Aortic Stenosis: ↓ in SP, PP and MAP

↓ in stroke volume

Aortic Regurgitation: Retrograde flow, can cause microangiopathic hemolytic anemia (mechanical destruction)

Explain the significance of the:

P wave

PR interval

PR segment

QRS complex

J point

P wave: atrial depolarization

PR interval: beginning of P wave to beginning of QRS complex; nml: 0.12 - 0.20; useful for diagnosing heart blocks

PR segment: end of P wave to beginning of QRS

QRS complex: ventricular depolarization and atrial re-polarization; nml: 0.08 - 0.10

J point: end of QRX complex and beginning of the ST segment; evaluated in near drowning, or in ST elevation or depression

Explain the significance of the:

QT interval

ST segment

T wave

U wave

QT interval: beginning of QRS to the end of the T;  ventricular depolarization, mechanical contraction of the ventricles and ventricular re-polarization; used to diagnose rhythm problems

ST segment: end of QRS to beginning of T,

should be isoelectric;

Depression indicates ischemia

Elevation indicates infarction

T wave: Ventricular Re-polarization (aortic valve closes?)

U wave: between T and P waves; re-polarization of Purkenje Fibers; changes are seen with hypokalemia and bradycardia

What is the effect of atropine on HR?

Propranolol? 

β-blockers?

↑ HR(blocks PNS)

Propranolol is a β-blocker

↓ HR (blocks SNS)

Without any input from the ANS, resting HR is 100 bpm

Used to estimate cardiac output from the differencce in oxygen concentiaont in the blood before it enters and afer it leaves the lung and from the rate at which oxygen is consumed

Q = (O₂ consumption rate) / (A-V difference)

[O₂]_a - [O₂]_v

[O₂]_a

1.) nml physiological splitting can be caused by inspiration

2.) Very wide splitting uninfluenced by respiration occurs with rapid emptying of the L ventricle (as in mitral valve insufficiency) or prolonged contraction of the R ventricle (as in Pulmonic Stenosis or R Bundle Branch Block)

3.) Paradoxical splitting (A₂ after P₂) can be caused by severe Aortic Stenosis, Left Bundle Branch Block, or severe Systemic HTN; inspiration minimizes splitting

1 - very faint, not heard in all positions

2 - soft, heard in all positions

3 - loud, no thrill

4 - loud w/ thrill

5 - heard w/ stethoscope partially off chest

6 - heard w/ stethoscope completely off chest

Systolic:

Aortic Stenosis 

Mitral Regurgitation

Diastolic:

Aortic Insufficiency

Mitral Stenosis

Systolic murmur (can be heard early or late)

Best heard at the 2nd intercostal space, R of the sternum

crescendo-decrescendo

Paradoxical splitting (P₂ before A₂)

Aortic pulse pressure weak

Sometimes radiates to carotid aa.

Diastolic murmur, begins at A₂

High pitched, decrescendo, "blowing"

Small systolic murmur also heard due to large volume ejected

Diastolic murmur

Low pitched, rumbling

Maximum loudness when atrium contracts

Decrescendo-crescendo

"opening snap" after S₂ followed by murmur

Can be caused by Streptococcal pharyngitis 

Systolic murmur, immediately after S₁

long in duration

Best heard at 5th intercostal space, in axilla, or at PMI

S₃ gallop

Wide splitting, P₂ after A₂

Confirm on US

A dimensionless number used to predict laminar or turbulent flow

N_R = ρdv/η

ρ = density of blood

d = diameter of blood vessel

v = velocity of blood flow

η = viscosity of blood

R = 8ηL/πr⁴

R = resistance in a give blood vessel

η = viscosity of blood

L = length of blood vessel

r = radius of blood vessel

Poiseuill-Hagen Q = π/8 · ΔPr⁴/ηL

Ventricular tachyarrhythmia caused by a mutation in sodium channel genes

Major cause of sudden of unexplained death due to cardiac failure

Tx: Implanted cardioverter-defibulator

1. Ejection fraction: ↑EF ⇒ ↑ contractility

2. Maximum dP/dt: faster PΔ ⇒ ↑ contractility

3.  Maximum ejection velocity: faster EV ⇒ ↑ contractility

4. ESPVR (End-Systolic Pressure-Volume Relation)

↑ slope ⇒ ↑ contractility

Contractility - the ability of muscle to generate tension at a given length

↑ Ca²⁺ current & ↑ Ca²⁺ stored in SR ⇒ ↑ contractility

End diastolic volume

Right atrial pressure

End diastolic pressure

Systole

Diastole

Ventricles contract;

occurs between

S₁ (mitral and tricuspid valve closure) and

S₂ (semilunar valve closure)

Ventricles relax;

Occurs between S₂ and S₁

usually lasts longer than systole

closely followed by atrial systole

Where re the 3 main barorecptors (mechanoreceptors) located in the body?

How are these receptors affected by increased pressure?

carotid sinus

aorta

afferent arterioles in kidney (RAAS)

As pressures increase, signal frequency/firing rate also ↑

If high pressures are sustained for long periods of time, receptors become desensitized

S₁ - closure of the atrioventricular valves, M & T

S₁ - closure of the semilunar valves, A & P

pulmonary closure is delayed during inspiraion, usually simultaneous, but can be split

S₃ - occurs in diastole (early), ventricular "gallop"

S₄

67% veins and venules

5% capillaries 

11% aorta, arteries, and arterioles 

Latent Pacemakers

Overdrive Suppression

Ectopic Pacemakers

Latent pacemakers have intrinsic automaticity (the capacity for spontaneous phase 4 depolarization)

Examples: AV node, bundle of His, Purkinje Fibers

The SA node has the fastest firing rate which suppresses the intrinsic automaticity in the latent pacemakers

If the SA node firing rate decrease, the firing rater of one of the latent pacemakers ↑, or the conduction of action potential is blocked a latent pacemaker may become the main pacemaker

Related to distensibility

C = V/P

or 

ΔC = ΔV/ΔP

aging and artherosclerosis cause a decrease in compliance

Active Hyperemia

Reactive Hyperemia

Autoregulatoin

Metabolic demand regulates flow

Ischemia promotes flow

As pressure ↑ vessel diameter ↓

(aka, myogenic effect)

Cardiac Output

Venous Return

Stroke Volume

CO = HR x SV = VR = MAP/TPR

CO: rate at which blood is pumped from either ventricle

VR: rate at which blood is pumped from the L ventricle, the rate at which blood is returned to the atria from the veins

SV: volume contained in vessels that are stretched

MAP = mean arterial resistance

TPR = total peripheral resistance

Stressed - volume contained in vessels that are stretched

Unstressed - volume contained under intrinsic compliance

Sudden shifting of blood volume to the skin decreases cardiac output.

Pt is also losing fluids through respiration and sweat, and may be hypovolemic

What is one (in-field) treatment of paroxymal supraventricular tachycardia (PSVT)?

Bradycardia?

Carotid massage ⇒ ↓ HR

Valsalva Maneuver ⇒ ↑ HR

(exhalation against a closed airway)

↑ MAP

↑ Pulse Pressure

↑ Systolic Pressure

↓ SV

↓ CO

↓ MAP PP and SP

may cause microangiopathic hemolytic anemia (mechanical destruction of RBCs)

Presents with photo-sensitivity and painful blistering 

More likely in older patients, no strong hereditary connection 

Deficiency in ferrocchelatase 

Urine: coproporphyric (COPRO) w/ hepatopathy

Stool, plasma, & RBCs: protoprophyrin (PROTO)

Presents as _____

Exacerbated by EtOH consumption

Deficiency in uroporphyrinogen decarboxylase

Urine and Plasma: uroporphyrin

Urine, Stool & Plasma: heptacarboxyl, porphyrin

RBCs: ZnPROTO

Stool: ISOCOPRO

Presents as (5Ps): Painful abdomen, Pink urine, Polyneuropathy, Psych disturbances, Precipitated by drugs

Deficiency in porphobilinogen deaminase

Tx: Glc & Heme

Urine & Plasma: aminolevulinic acid (ALA), porphobilinogen (PBG), uroporphyrin (URO1)

Stool: normal, COPRO1

RBCs: ↓ PBGD

Q = K_f [(P_c - P_i) - σ(π_c - π_i)]

Q = flow

K_f = hydraulic conductance or filtration coefficient

P_c = hydrostatic pressure in the capillary

P_i =  hydrostatic pressure in the interstitium

σ = correction factor

π_c = osmotic pressure in the capillary

 π_i = osmotic pressure in the interstitium

π_s = RTC_s

R =  8.314 J/mol·K

T = absolute temperature

relates oncotic pressure to concentration for a given substance, s

What is the affect of ANP on the blood volume?

BNP?

ANP - atrial natriuretic peptide

BNP - brain natriuretic peptide

both cause vasodilation in kidneys → ↑ Na⁺ & H₂O

released in response to activation of stretch receptors

Postganglionic axons enter the renal plexus and are distributed along renal vasculature including the juxtaglomerlar cells

SNS stimulation causes increased renin release, which stimulates production of angiotensin I → angiotensin II ⇒ increased BP and Na⁺ retention

Aortic and carotid baroreceptors stimulate the nucleus tractus solitarius ⇒ vasocontrictin; the baroreceptors also causes a Δ in I_f (SA node) ⇒ ↑ HR & contractility

(alter SERCA activity)

Names some agonists and antagonists for α₁ receptors

What does stimulation of α₁ receptors cause?

agonists:

Norepinephrine, Phenylephrine

antagonists:

Phenoxybenzamine, Phentolamine, Prazosin

Contraction/Constriction of smooth muscle in blood vessels, skin, kidneys, throughout GI, sphinters

IP₃ ⇒ ↑ intracellular Ca²⁺

agonists:

Clonidine

antagonists:

Yohimbine

Names some agonists and antagonists for β₁ receptors

What does stimulation of β₁ receptors cause?

agonists:

Norepinephrine, Epinephrine, Isoproternol, Dobutamine

antagonists:

Propranolol, Metoprolol

↑ HR and conductivity (GTP coupled, ↑ [Ca²⁺])

↑ renin secretion in the kidney (↓cAMP)

salivary glands

Names some agonists and antagonists for β₂ receptors

 What does stimulation of β₂ receptors cause?

agonists:

Epniphrine (preferred), Norepinephrine, Isoproternol, Albuterol

antagonists:

Propranolol, Butoxamine

Relaxation/Dilation in bladder wall, vascular mm, throughout GI tract, and in brochioles 

↑ cAMP

agonists:

ACh, Nicotine

antagonists:

Curare, Hexamethonium

Names some agonists and antagonists for muscarinic receptors

 What does stimulation of muscarinic receptors cause?

agonists:

ACh, Muscarine

antagonists:

Atropine

↓ HR (SA node) & conduction velocity (AV node)

all 11-cis rhodopsin is converted to all-trans rhodopsin

The G protein transducin is activated

phosphodiesterase is activated, and stimulates the breakdown of cGMP

decreased cGMP levels cause Na⁺ gates to close, leading to the hyperpolarization of the photoreceptor

an inhibitory or stimulatory neurotransmitter is released

Caused by a gain-in-function mutation in RyRs that leads to increased Ca²⁺ from SR

Usually an episode precipitated after anesthesia is given to the patient