Clin Med Exam 6 - Cardiology

most common cause of death worldwide even before cancer

CAD

what maneuvers decrease venous return?

standing, valsalva

with what maneuvers will you best hear mitral valve prolapse?

standing and valsalvaw

what maneuvers increase venous return?

squatting, leg raise, lying down

with what maneuvers will you best hear aortic stenosis and regurgitation?

squatting, leg raise, lying down (increase venous return)

when do you best hear HOCM?

standing and valsalva

inspiration makes what.murmurs sound louder?

right side (tricuspid and pulmonic)

expiration makes what murmurs sound louder?

left side (mitral and aortic)

ACE inhibitors, CHF/pulmonary edema can cause what symptom?

cough

pulmonary hypertension due to severe left sided HF can cause what symptom?

hemoptysis

CAD, severe valvular disease with aortic stenosis, HOCM, vasovagal, cardiac arrhythmia, orthostatic hypotension, can cause what neuro symptom?

dizziness or syncope

HOCM

hypertrophic obstructive cardiomyopathy

endocarditis might present with what non-cardiac symptoms?

fever and chills

rheumatic fever cardiac symptoms

tachy, cardiomegaly, new murmur, pericardial friction rub, muffled heart sounds, chest pain (from carditis)

peripartum cardiomyopathy signs/symptoms

new onset of SOB, DOE, edema

what drugs can increase systemic blood pressure?

OTC cough medications, decongestants, NSAIDs, stimulants, oral contraceptives

what cardiac condition might splinter hemorrhages, osler nodes, and janeway lesions suggest?

endocarditis

Levine's sign

clenched fist against chest

sitting upright, leaning forward unable to fly flat due to chest pain might indicate?

pericarditis

abnormal JVP

>5cm

S1

the first heart sound, heard when the atrioventricular (mitral and tricuspid) valves close - "lub"

S2

second heart sound, heard when the semilunar valves (pulmonary and aortic) valves close - "dub"

S3

an abnormal heart sound detected early in diastole as resistance is met to blood entering either ventricle; most often due to volume overload associated with heart failure

ventricular gallop → early diastolic passive ventricular filling (systolic HF)

S4

atrial gallop → late active ventricular filling as the atrium contracts against stiff ventricle (diastolic dysfunction)

a pericardial friction rub on exam is indicative of?

acute pericarditis

rales (crackles) indicating fluid in the alveoli are seen in what heart conditions?

CHF/pulmonary edema

pericardium

Double-layered membrane surrounding the heart.

epicardium

outer layer of the heart

what makes up the majority of the heart's mass?

myocardium

what layer of the heart lines the chambers, valves, vessels?

endocardium

describe the flow of blood through the heart

Superior and inferior vena cava --> R atrium --> tricuspid valve --> R ventricle --> pulmonary valve --> pulmonary artery --> lungs --> pulmonary vein --> L atrium --> mitral valve --> L ventricle --> aortic valve --> aorta --> systemic circulation

what supplies the myocardium?

coronary arteries

When do the coronary arteries fill with blood?

during ventricular diastole

Why don't the coronary arteries fill during systole?

because the pressure in the coronary arteries is higher than in the aorta during systole, so blood doesn't flow through them

What collects deoxygenated blood from the myocardium?

the coronary sinus vein

Where does the coronary sinus drain the deoxygenated blood?

the right atrium

Where is the coronary sinus located?

in the sulcus between the left atrium and left ventricle on the posterior surface of the heart

electrical system of the heart

SA node --> AV node --> bundle of His --> bundle branches --> Purkinje fibers

where is the SA node located? what does it set the sinus rhythm to?

right atrium

60-100 bpm

what is Bachmann's bundle?

a portion of the cardiac conduction system found in the left atria.

It is connected to the SA node and allows for simultaneous contraction of the atrias.

where is the internodal pathway and what does it do?

Located in the right atrium

Receives action potential from SA node and depolarizes the right atrium together with the SA node

what does the AV node do?

located between the atria and ventricles --> slows electrical conduction from atria to ventricles to allow for ventricular filling before ventricles contract

Allows for depolarization to come from the atria down to the ventricles

what does the PR interval represent?

the time required for the impulse to travel from the atria through the AV node (AV node delay for ventricular filling)

carries electrical signals from the AV node to the Purkinje fibers in the ventricles

Bundle of His

Located in the subendocardial surface of the ventricle walls (part of the endocardium)

Receive electrical signals from the Bundle of His to the ventricles to contract

Purkinje fibers

what does it mean that pacemaker cells have automaticity?

they have the intrinsic ability to spontaneously depolarize and trigger action potential for ventricular cells to contract the heart's muscle (myocardium)

what rate can the AV node maintain should the SA node fail?

40-60 bpm

what rate can the Bundle of His and Purkinje fibers maintain should the SA and AV node fail?

20-40 bpm

what are ventricular cells vs pacemaker cells?

Ventricular cells: contractile cells (myocytes) that responds to the electrical signal generated by the pacemaker cells and cause forceful contraction

Pacemaker cells: noncontractile, specialized cells that spontaneously generate electrical impulses to initiate the heartbeat → contraction → pumping of blood

where are ventricular cells found?

in the myocardium of the heart

ventricular vs pacemaker cell action potential and depolarization

ventricular: fast response action potential with rapid depolarization phase

pacemaker: slow response action potential with gradual depolarization phase

What is the resting membrane potential of ventricular cells?

about -90 mV due to high permeability to potassium ions at rest

Do pacemaker cells have a stable resting membrane potential? how do they depolarize?

No, they have a pacemaker potential that slowly depolarizes due to If (funny) channels

What causes the slow depolarization in pacemaker cells?

If (funny) channels

What causes the rapid depolarization (Phase 0) in ventricular cells?

a large influx of sodium ions through voltage-gated Na+ channels

What ion is responsible for depolarization in pacemaker cells?

calcium influx through slow Ca2+ channels

What ion is responsible for repolarization in both ventricular and pacemaker cells?

Potassium (K+) efflux (leaving the cell)

What gives pacemaker cells automaticity?

The spontaneous depolarization caused by If (funny) currents

Why do ventricular cells have a long refractory period?

To prevent tetany and allow diastolic filling (relaxation)

Why do pacemaker cells have a shorter refractory period?

To maintain regular rhythmic firing of the SA node (60-100 bpm)

What occurs during Phase 1 of the ventricular action potential?

initial repolarization as Na+ channels close and K+ begins to leave the cell via fast K+ channels

What causes the plateau phase (Phase 2) in ventricular cells?

Ca2+ influx through slow Ca2+ channels and decreased K+ efflux

What occurs during Phase 3 of the ventricular action potential?

Rapid repolarization as Ca2+ channels close and K+ permeability increases (slow K+ channels open)

What is Phase 4 in ventricular action potentials?

Resting membrane potential (about -90 mV), maintained by K+ permeability.

Do pacemaker cells have a stable resting membrane potential?

no, there is just slow depolarization

Which channels are responsible for the pacemaker potential in Phase 4?

If (funny) channels

When do If channels open in pacemaker cells? when do they close?

(If) channels are open at about -60 mV until membrane hits threshold -40 mV to action potential, then they close

At what membrane potential do voltage-gated Ca2+ channels open in pacemaker cells?

At -40 mV (the threshold)

What is Phase 0 of the pacemaker action potential characterized by?

Opening of voltage-gated Ca2+ channels and rapid calcium influx

what causes depolarization of pacemaker cells?

opening of Ca2+ channels when threshold is reached

what occurs during Phase 3 in pacemaker cells?

repolarization due to potassium (K+) efflux through voltage-gated K+ channels

ectopic pacemaker cells

excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart

can cause irregular heart beats/arrhythmias

threshold pacemaker vs ventricular

pacemaker: -40mV

ventricular: -70mV

primary depolarization ion pacemaker vs ventricular

pacemaker: Ca++

ventricular: Na+

membrane potential pacemaker vs ventricular

pacemaker: unstable -60mV (oscillates)

ventricular: stable, -90mV

what is the most influential ion in setting the resting membrane potential of cardiac cells and why?

potassium

due to cardiac cells being highly permeable to K+ at rest

RMP is primarily maintained by the ___________ gradient across the cell membrane

potassium

what will mild hyperkalemia show on EKG?

Peaked T waves due to faster repolarization of the ventricle (most prominent in precordial leads)

how does mild hyperkalemia affect the EKG and why?

Hyperkalemia makes the resting membrane potential less negative (depolarized a bit) --> more K+ in cell

Voltage-gated K⁺ channels are sensitive to voltage — and when the cell is less negative, these open earlier and more easily.

more K⁺ channels activate earlier, speeding up Phase 3 repolarization.

Result → peaked T waves (faster repolarization).

how does moderate hyperkalemia affect the EKG?

prolonged PR interval (slowed AV conduction)

widened QRS complex due to slowed ventricular conduction

this is due to inactivated Na+ channels as a result of higher RMP because of higher extracellular K+

how does moderate hyperkalemia result in bradycardia?

With both AV node and ventricular conduction slowing down, and SA node activity sometimes suppressed, the overall heart rate slows

what is seen on EKG in severe hyperkalemia and why?

Loss of P waves due to atrial depolarization is suppressed (Na+ channels are closed due to higher RMP, no Na⁺ influx = no depolarization = no P wave)

Sine wave pattern (fusion of QRS and T waves, pre-terminal rhythm that can lead to deadly ventricular arrhythmias or asystole → cardiac arrest)

severe hyperkalemia

>7.5

sine wave EKG

Normally, the QRS complex (ventricular depolarization) and T wave (ventricular repolarization) are separate, distinct parts of the EKG.

In severe hyperkalemia:

The QRS becomes so wide and distorted due to extremely slow conduction.

The T wave becomes tall and merges with the QRS.

what happens to the RMP in hypokalemia?

increase in K+ efflux making the RMP more negative (hyperpolarization) - depolarization more difficult as the cells are further from threshold

what happens the RMP in hyperkalemia?

decrease in K+ efflux making the RMP less negative (depolarization of the cell)

- cells are closer to the threshold for depolarization but may fail to fully repolarize

describe what you will see on EKG as potassium levels rise? (end with cardiac arrest)

1. peaked T waves

2. PR interval prolongation and flat and wide p waves

paroxysmal atrial fibrillation

< 7 days

AF that terminates spontaneously or

with intervention within 7 days of onset

persistent atrial fibrillation

< 1 year

AF that fails to self-terminate within 7

days but does not exceed 12 months

long standing persistent atrial fibrillation

> 1 year

AF that has lasted for more than 12

months

Individuals with long standing atrial fibrillation

where a joint decision by the patient and

clinician has been made to no longer pursue a

rhythm control strategy.

permanent (chronic) atrial fibrillation

Wenkebach

Nickname for second degree AV block type I

Progressive prolongation of the PR Interval

culminating in a non-conducted P wave

The PR interval is longest before the dropped beat

and shortest immediately after the dropped beat.

2° AVB

Mobitz I

(Wenkebach)

PRI> 200ms (five small squares)

Severe if PR interval > 300ms

1° AVB

Intermittent non-conducted P waves without

progressive prolongation of the PR interval.

The PR interval in the conducted beats remains

constant.

The RR interval is an exact multiple of the

preceding RR interval

2° AVB

Mobitz II

(High Grade)

Complete absence of AV conduction - none of the

supraventricular impulses are conducted to the

ventricles.

Perfusion sometimes maintained by a junctional or

ventricular escape rhythm.

P waves often seen "marching through"

3° AVB

(Complete)

intervention for 3° AVB

pacemaker

advantages of VVI pacemaker setting

useful for AF and high grade AV block

what is the AAI pacemaker setting able to detect?

ST changes

with which pacemaker setting is AV synchronicity lost?

VVI